As a result, PDAC-DM has often been assumed to pathologically mirror type 2 diabetes, and the field has been fractured around inconsistent disease descriptions—glycaemic dysregulation, glycaemic dysfunction, insulin-sensitive, insulin-deficient, new-onset diabetes (NOD), or type 3c diabetes—without a shared, mechanistic vocabulary [3,4,5]. This evidence concerns the gene INS and dentatorubral-pallidoluysian atrophy.