Interestingly, in an animal model of NASH progressing to HCC in the absence of an exogenous carcinogen, and therefore more closely resembling the natural course of human disease, miR-155 was found to be significantly upregulated at early stages of hepatocarcinogenesis, in parallel with reduced expression of its target CCAAT/enhancer binding protein beta (C/EBPβ). This evidence concerns the gene CEBPB and metabolic dysfunction-associated steatohepatitis.