PRDM9 and hepatocellular carcinoma: However, miR-122 is decreased in HBV infection and when genetically deleted in mice results in spontaneous hepatosteatosis, inflammation, fibrosis, and HCC.26,27 HBx represses miR-122 by recruiting peroxisome proliferator-activated receptor gamma (PPARγ) and its associated SUV39H-containing corepressor complex to the miR-122 promoter.28 Hence, altered expression or mutation of histone methyltransferase genes in HCC disrupts multiple regulatory networks, including a large number of miRNAs involved in posttranscriptional control.