Increased Metrnl promoted browning of white adipose tissue via an eosinophil‐dependent increase in IL4 expression and M2 macrophage activation, and thus stimulated energy expenditure and improved glucose tolerance.11 Li et al13 demonstrated that overexpression of Metrnl in adipocytes upregulated PPARγ expression, which in turn inhibited adipose inflammation, enhances adipocyte differentiation, activates lipid metabolism, and ultimately reduced insulin resistance. Here, METRNL is linked to Insulin resistance.