In this setting, the cJun NH2-terminal kinase (JNK) stress-signaling pathway, involved in BA metabolism, has recently gathered attention not only due to the improvement in steatosis and IR obtained after its inhibition [118] but also because JNK deficiency leads to an increased risk of biliary cells inflammation and the development of intrahepatic cholangiocarcinoma, as demonstrated in rats [119]. Here, MAPK8 is linked to steatosis.