Moreover, we demonstrated, for the first time, that the PG, similarly to that observed in other organs 31, develops a drastic insulin resistance in conditions of obesity, as demonstrated by the severely reduced increments of AKT phosphorylation in response to an acute insulin injection, thus reinforcing the idea of a relevant crosstalk between the alterations in the endocrine–metabolic status (i.e. obesity) and the dysregulation of the normal metabolic homeostasis of the PG. The gene discussed is INS; the disease is obesity disorder.