Together with findings by others, our results support the hypothesis that LL‐37 secreted by pancreatic β‐cells or infiltrated neutrophils under conditions of pancreatic inflammation binds IAPP and suppresses its amyloid self‐assembly and related β‐cell damage, thus slowing down T2D pathogenesis (Scheme 2).2a, 2c, 4a Studies on the potential physiological relevance of the LL‐37/IAPP interaction are now of high priority. The gene discussed is CAMP; the disease is type 2 diabetes mellitus.