The mechanisms behind the anti‐obesity effects of hAMSCs‐CM may involve the inhibition of lipid synthesis and adipogenesis mediated by PPARγ and C/EBPα, the enhancement of glucose metabolism through GLUT4, the elevation of energy expenditure regulated by UCP1/PPARα/PGC1α, and the promotion of M2‐type macrophage polarisation via STAT3‐ARG1 signalling [37]. The gene discussed is PPARGC1A; the disease is obesity disorder.