Subsequent in vitro experiments showed that compared with the inhibitory effect on adipogenesis via activation of canonical Wnt signalling mediated by Wnt1 and Wnt10b, Wnt5b was overexpressed in 3T3‐L1 cells at an early phase of adipogenesis and could stimulate adipogenesis by antagonizing the canonical Wnt pathway,99, 100 suggesting that Wnt5b may contribute to the susceptibility to T2DM; therefore, down‐regulation of non‐canonical Wnt5b pathway could therefore decrease adipogenesis and increase β‐cell functions of T2DM subjects. The gene discussed is WNT1; the disease is type 2 diabetes mellitus.