First, tumourigenesis after c-Myc activation is initiated and proceeds by different routes, with inherent pro-apoptotic activity avoided by an additional genetic alteration (expression of the anti-apoptotic protein, BclxL) as is the case in the islet tumourigenesis model, or by the presence of survival cues in the microenvironment, as seen in c-Myc-induced skin tumours. Here, MYC is linked to skin neoplasm.