Conversely, Mo-Mφ in the NASH-HCC model displayed a distinct phenotype, characterized by a mixed pro-inflammatory expression profile and the upregulation of immunomodulatory (Tlr4, Tlr6, Mtor, Ada) and lipid metabolic (Apoc2, Apob, Scd1) genes [55]. This evidence concerns the gene APOB and metabolic dysfunction-associated steatohepatitis.