Three genes (ELK4, SULT1A2, and WFS1) were prioritized as druggable targets, with COMPOUND 5G and DCLK1-IN-1 emerging as potential therapeutic agents through computational analyses.<h4>Conclusion</h4>Our study reveals novel genetic associations and immune-related pathways in T1D pathogenesis, and proposes specific genes and compounds as promising focal points for future mechanistic and therapeutic exploration. This evidence concerns the gene SULT1A2 and type 1 diabetes mellitus.