A GWAS utilizing data from the UK Biobank identified 496 shared risk SNPs, implicating critical biological pathways involved in both disorders, including glycolipid metabolism (PPAP2B, DGKB, LIPC), adipocytokine signaling (LEPR, PPARGC1A), T2DM (GCK, CACNA1C), long-term depression (ITPR2, IGF1), and immune pathways (NFATC3, NFATC2) (37). This evidence concerns the gene LEPR and type 2 diabetes mellitus.