Accumulating evidence suggests that T1D risk genes interplay with viral infections in pancreatic β cells, promoting an imbalanced antiviral and pro‐inflammatory response that culminates in the autoimmune destruction of insulin‐producing cells.[3, 4, 5, 6] Indeed, the role of viral infections in T1D development is supported by clinical and epidemiological data.[7, 8, 9, 10, 11, 12]. This evidence concerns the gene INS and viral infectious disease.