Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system and a leading cause of disability in young adults, with no known cure. Although the exact etiology of MS remains unclear, genome - wide association studies ( GWAS) have significantly advanced our understanding of its causes. Large-scale GWAS have identified 236 genetic variants associated with increased risk of MS, most of which are non-coding. These variants may be related to the role of adaptive and innate immune cells in the pathogenesis of MS, providing crucial biological insights into the etiology and mechanisms of the disease. Additionally, some MS-related variants also mediate the risk of other autoimmune diseases. This paper reviews the genetic susceptibility to MS, the role of recently discovered neuroimmune-related genetic variants in its pathogenesis, and their association with other autoimmune diseases. Finally, the paper discusses how these genetic risk variants influence the development of new drugs and the application of individual genetic information to personalized treatments.