Among these potential mechanisms of SOCS1-mediated tumor suppression, only the attenuation of the pro-oncogenic capacity of CDKN1A has been genetically proven in our earlier study, wherein we demonstrated that the simultaneous ablation of the Cdkn1a gene attenuated HCC induction by the genotoxic hepatocarcinogen diethyl nitrosamine (DEN) in hepatocyte-specific SOCS1-deficient mice [32]. The gene discussed is SOCS1; the disease is hepatocellular carcinoma.