In more detail, impaired insulin ability to inhibit lipolysis processes in peripheral adipose tissue leads to increased levels of FFAs and elevated intrahepatic diacylglycerol concentrations, which are associated with activation of the protein kinase C epsilon (PKC-ε) and c-Jun N-terminal kinases 1 (JNK1) pathways, affecting insulin receptor substrates 1 and 2 and eventually aggravating insulin resistance and liver steatosis [50,51]. The gene discussed is INS; the disease is Hepatic steatosis.