CDKN2A and neoplasm: Also in the case of malignant transformation by oncogenes, Miliani de Marval et al. reported that lack of CDK4 expression due to gene knockdown in K5Myc transgenic mice resulted in the complete inhibition of tumour development, induced by deregulated Myc, suggesting that CDK4 is a critical mediator of tumour formation28 Furthermore, transformation in response to Ras activation with dominant‐negative (DN) p53 expression or in an Ink4a/Arf‐null background does not occur in CDK4‐null mouse embryonic fibroblasts, providing a further indication that Cdk4 is essential for immortalisation.29