Signaling pathways leading to HCC in Gnmt KO mice. Loss of GNMT activity induces an abnormal accumulation of hepatic AdoMet leading to a major epigenetic alteration in gene expression regulation. These epigenetic changes include the hypermethylation of Rassf1 and Socs2 promoters, as well as the trimethylation of histone 3 lysine 27 associated with these genes. As a consequence, the expression of Rassf1 and Socs2, as well as of other inhibitors of Ras and JAK/STAT signaling pathways, is downregulated. This leads to the activation of Ras and JAK/STAT signaling pathways, to abnormal growth, and to malignant transformation.