This overexpression may exacerbate T1DM pathogenesis through several mechanisms: it promotes the survival of autoreactive T‐cells by inhibiting apoptosis‐related genes like PDCD4, enhances inflammatory cytokine production via the STAT3 and NF‐κB pathways, and increases beta‐cell susceptibility to cytokine‐induced apoptosis. This evidence concerns the gene NFKB1 and type 1 diabetes mellitus.