Thus, the released prolactin in mice consuming a high‐fat diet (HFD) can mitigate hepatic steatosis through its interaction with the hepatic prolactin receptor (PRLR) and by modulating the expression of CD36, a pivotal fatty acid translocase (FAT) of free fatty acid (FFA) uptake. The gene discussed is PRLR; the disease is Hepatic steatosis.