The liver model provides insights into a RAS dose-associated evolution of senescence and immune microenvironment, revealing at least two distinct paths towards tumorigenesis in the liver: the Dlk1/Afp branch, corresponding to differentiated HCCs with longer latency, and the Notch1/Tgfb1/Nes branch, corresponding to undifferentiated tumours and associated with short latency and poor prognosis. Here, AFP is linked to neoplasm.