Interestingly, a recent study18 published in Arteriosclerosis, thrombosis and vascular biology provided the first direct evidence that SFRP5 exerted its restorative effect on the WNT5A‐induced endothelial dysfunction through the inhibition of the WNT5A/JNK pathway and the up‐regulation of endothelial nitric oxide production, which suggests a possible role of SFRP5 as a protective factor in the development atherosclerosis under conditions of metabolic dysfunction. The gene discussed is SFRP5; the disease is atherosclerosis.