Other underlying mechanisms clearly implicated in the development of hepatic IR and in the progression of NAFLD are low-grade chronic inflammation, elevated production of reactive oxygen species, activation of unfolded protein response and endoplasmic-reticulum stress, activation of Jun N-terminal kinase (JNK)-1, increased hepatocyte apoptosis and lipo-autophagy [25,92,102,123,124,125,126,127]. Here, MAPK8 is linked to metabolic dysfunction-associated steatotic liver disease.