MAPK1 and steatosis: Knockout experiment of liver-specific p38α in mice resulted in reduced hepatomegaly.[123] p38γ and p38δ knockout mice display hepatosteatosis resistance in HFD as well as MCD diet mice.[124] In both studies, p38 is important in driving chronic inflammation to induce liver damage, with p38γ and p38δ responsible for neutrophil migration to the liver to induce steatosis, as well as p38α upregulating proinflammatory cytokines expression.[123,124] As such, p38 isoforms are also important in the driver of hepatic diseases.