Could One Gene Predict MS Treatment Success? A New Study Says Yes, for This Drug

A team of researchers recently published findings that could help doctors make better decisions when choosing treatments for multiple sclerosis (MS). The study, published in the European Journal of Neurology, looked at a single genetic variant—rs7665090—and found that it may predict how well patients respond to interferon-beta (IFNβ) [1], one of the most commonly used MS drugs. And the results were quite unexpected.

At this juncture, it’s worth noting that MS remains one of the most challenging neurological diseases to treat. Over 2.9 million people worldwide live with the condition [2], which is characterized by an unpredictable mix of relapses, progression, and variable symptoms, ranging from vision problems to fatigue, muscle weakness, and numbness. While there’s no cure yet, dozens of disease-modifying therapies (DMTs) are available to slow progression and reduce relapses. 

But here’s the catch: not all patients respond the same way, and trial-and-error still dominates the treatment process.

A Closer Look at the rs7665090 Variant

For years, researchers have been trying to decode why some people with MS respond well to interferon-beta while others don’t. A 2015 review published in Cytokine & Growth Factor Reviews summarized dozens of these efforts and concluded that, despite promising signals, no single genetic marker had emerged as a consistent predictor of treatment response [3]. Different studies used different patient populations, different definitions of response, and different genotyping methods, making it difficult to compare results or apply them clinically.

In other words, pharmacogenomics in MS had promise but no payoff. Until now, perhaps.

This new study offers something that’s been missing from the conversation: a clear, statistically significant association between a single genetic variant—rs7665090—and real-world treatment outcomes with interferon-beta [4]. 

Unlike earlier studies, this one had a relatively large sample size (558 patients), used a standardized outcome measure (the Rio Score), and controlled for key confounding variables. Most importantly, it focused on a variant already known to affect immune activity, giving the findings biological plausibility.

Details of the study

Researchers examined 558 people with relapsing MS, all of whom had been genotyped to identify their version of the rs7665090 gene. They then grouped these patients according to the type of MS treatment they were receiving—injectables like interferon-beta and glatiramer acetate, oral drugs like dimethyl fumarate (DMF), teriflunomide, and fingolimod, or monoclonal antibody therapy like natalizumab. Their aim was to see whether the rs7665090 genotype could predict treatment success.

Turns out, it could, at least for one drug. 

Among patients treated with IFNβ, those who had the GG genotype at rs7665090 were significantly more likely to respond well. In fact, the odds of not responding were 58% lower in this group compared to other genotypes. Importantly, this association held even after adjusting for age, baseline disability, and other variables. No such effect was seen in patients treated with the other drugs.

Now, this might seem counterintuitive. 

The GG genotype has previously been linked to increased immune activity via the NFκB pathway, which is generally thought to be pro-inflammatory. You’d expect that to worsen disease activity, not improve treatment response. Yet here it seems to do the opposite, at least when it comes to interferon-beta. It’s a reminder that immune signaling in MS is complex, and what looks “bad” on one level might actually help predict who benefits from a specific therapy.

Why This Finding Could Shift the MS Treatment Conversation

IFNβ is still widely used, especially in countries or health systems where newer drugs are less accessible or affordable. Having a genetic marker that can tell you upfront whether a patient is likely to benefit from it would be incredibly useful, not just for tailoring treatment, but also for sparing patients the frustration of failed therapies and unnecessary side effects.

Of course, this is just the beginning. The study authors point out that these findings need to be validated in larger, ideally prospective, cohorts. But the implications are clear: genotyping for rs7665090 might one day become part of routine care in MS clinics. This is especially the case for patients considering interferon-beta. 

It’s a small but meaningful step toward a future where MS treatment is guided by the patient’s unique genetic blueprint.

So is rs7665090 the crystal ball we’ve been waiting for in MS therapy? Not quite. But it’s one of the first solid hints that personalized medicine in MS is necessary and achievable!

For additional great articles, go here.

References

1. Filipi, M., & Jack, S. (2020). Interferons in the Treatment of Multiple Sclerosis: A Clinical Efficacy, Safety, and Tolerability Update. International journal of MS care, 22(4), 165–172. https://doi.org/10.7224/1537-2073.2018-063
2. Walton, C., King, R., Rechtman, L., Kaye, W., Leray, E., Marrie, R. A., Robertson, N., La Rocca, N., Uitdehaag, B., van der Mei, I., Wallin, M., Helme, A., Angood Napier, C., Rijke, N., & Baneke, P. (2020). Rising prevalence of multiple sclerosis worldwide: Insights from the Atlas of MS, third edition. Multiple sclerosis (Houndmills, Basingstoke, England), 26(14), 1816–1821. https://doi.org/10.1177/1352458520970841
3. Carlson, R. J., Doucette, J. R., Knox, K., & Nazarali, A. J. (2015). Pharmacogenomics of interferon-β in multiple sclerosis: what has been accomplished and how can we ensure future progress?. Cytokine & growth factor reviews, 26(2), 249–261. https://doi.org/10.1016/j.cytogfr.2014.10.008
4. Vilaseca, A., Urcelay, E., Malhotra, S., Castillo, M., Aroca, M., Vidal-Jordana, A., Pappolla, A., Carvajal, R., Arrambide, G., González-Jiménez, A., Gómez-Delgado, I., Cobo-Calvo, A., Mongay-Ochoa, N., Rodriguez-Acevedo, B., Tur, C., Villacieros-Álvarez, J., Ariño, H., Castilló, J., Zabalza, A., Midaglia, L., … Comabella, M. (2025). The Variant rs7665090 Is Associated With Interferon-Beta Response in Multiple Sclerosis Patients. European journal of neurology, 32(7), e70227. https://doi.org/10.1111/ene.70227