Genetics

This blog post reviews Lioudyno et al. (2020), which investigates whether the KCNA3 promoter polymorphism rs2821557—implicated in increased Kv1.3 potassium channel activity—modifies the rate of disability progression in multiple sclerosis rather than disease susceptibility. Using MSSS-based stratification of progression severity alongside flow-cytometric immune profiling, the study reports an enrichment of severe progression among minor C allele carriers and identifies higher frequencies of CXCR3+ effector memory CD4+ T cells in these individuals, offering a mechanistically plausible bridge between genotype and neuroinflammatory trajectory. The post synthesizes the study’s rationale, methods, key findings, and translational implications while emphasizing constraints such as cohort size and the need for independent replication.