Although we have shown that in CRC cells KRAS directs and is required to maintain transcriptional silencing of INK4A-ARF, in primary cells oncogenic signals (such as activated KRAS) induce transcription of INK4A-ARF, which leads to p53 and Rb pathway activation and ultimately growth arrest (Sherr, 2012). The gene discussed is KRAS; the disease is colorectal carcinoma.