Likewise, Wnt5a is highly expressed in ischaemic muscles and ECs from mice overexpressing glutaredoxin‐1, an oxidation‐promoting enzyme which is increased in T2DM patients, and exogenous Wnt5a treatment could inhibit the revascularization in hind limb ischaemia via activating the non‐canonical Wnt pathway,92 indicating a deleterious role of Wnt5a in diabetic foot. Here, WNT5A is linked to type 2 diabetes mellitus.