Enteric nervous system (ENS) plasticity with early obesity has been described in mice, with gastric motility consequences.31 As ENS and PINS have the same embryologic origin and that PINS is usually considered as the pancreatic prolongation of ENS to which it is still connected by entero‐pancreatic neurons,32 we hypothesized that in addition to what occurs in ENS, early obesity could lead to plasticity of PINS, contributing to the alteration of insulin secretion. The gene discussed is GPSM2; the disease is obesity due to melanocortin 4 receptor deficiency.