ATP1B1 and hyperinsulinemic hypoglycemia, familial, 4: In at least one study comparing the genomic and molecular characteristics of young onset pancreatic cancer versus average onset disease, distinct features such as the higher prevalence of K‐RAS wildtype status and enrichment of targetable mutations (ETV6‐NTRK3, TPR‐NTRK1, SCLA5‐NRG1, ATP1B1‐NRG1 fusions, IDH1 R132C mutation, and mismatch repair deficiency) were identified.19