This role was initially demonstrated by (i) increased tumor formation in Δex8 mice in the one-step DMBA skin carcinogenesis model, (ii) decreased p21WAF expression in Δex8 H-Ras-G12V-transformed MEFs, (iii) increased colony formation of H-Ras-G12V-transformed Δex8 primary cells, and (iv) finally explained by phosphorylation of p53 by PRAK at serine residue S37 [6]. The gene discussed is HRAS; the disease is neoplasm.