Recent studies showed that increased secretion of Wnt5a by enlarged adipocytes in the obese state could block insulin signalling and cause glucose intolerance via activating the non‐canonical Wnt5a/PCP pathway and systemic inflammation,75, 77 and an obviously positive correlation between the up‐regulated Wnt5a/PCP pathway and profound vascular insulin resistance were observed in visceral adipose tissue arterioles of obese individuals.78 The gene discussed is WNT5A; the disease is Glucose intolerance.