Furthermore, similar to the situation in cervical cancer, strong upregulation of p16INK4a protein expression obviously reflects a subset of tumours in which the p16INK4a-mediated control of cell cycle progression by regulation of the phosphorylation status of pRb is bypassed by genetic alterations of other essential components of the cell cycle control machinery. The gene discussed is CDKN2A; the disease is cervical carcinoma.