55. Furthermore, cellular transformation induced by Ras requires c-Jun 56, and c-Jun protects early stages of hepatocellular carcinomas in mice against apoptosis 57. C-Jun mediates its proliferative effects through suppression of tumour suppressors, such as p53 and p21WAF1, while triggering positive cell cycle regulators, such as CDK’s and Cyclins 58–59. We propose an important role for the AP-1 components that drive HCEC cell cycle progression. Thus, targeting AP-1 components, such as ATF2, seems to be an efficient therapeutic strategy 60. The gene discussed is JUN; the disease is neoplasm.