Together, our data suggest that, in the PGK- and UBC-NRASG12V models, a relatively high level of RAS can induce either senescence or a progenitor-like state (Notch1 and Nes), the latter leading to aggressive undifferentiated tumours, whereas a low level of RAS induces a distinct progenitor-like state (Dlk1, Gpc3 and Afp), developing more differentiated HCC with a longer latency period. The gene discussed is UBC; the disease is neoplasm.