In hepatocellular carcinoma, instances of functional impairment stemming from mutations affecting suppressive regulators of PPAR-γ, such as histone deacetylase 3 (HDAC3) and nuclear hormone corepressor (N-CoR), engender a propensity toward steatosis and aberrant hepatic expansion, ultimately culminating in malignancy in both murine models and human subjects [9, 10]. This evidence concerns the gene HDAC3 and steatosis.