ANGPTL8 and Hepatic fibrosis: This finding marks a breakthrough in overcoming the limitations of previous studies that primarily linked serum ANGPTL8 levels to liver macrophage PIRB‐mediated liver fibrosis.[23] We demonstrated that ANGPTL8, an extrahepatic effector, drives kidney fibrosis via macrophage PIRB signaling, a mechanism that is distinct from its autocrine/paracrine action in the liver.