For instance, p16 stays high in cervical cancer upon HPV E6-mediated inactivation of p53 function or lymphomas that overcame OIS or reprogressed out of TIS due to loss of intact p53 alleles, irrespective of p16’s ability to inhibit CDK4 and CDK6 (Carozzi et al., 2008; Fu et al., 2003; Sandhu et al., 2000; Schmitt et al., 2002; Braig et al., 2005). The gene discussed is CDKN2A; the disease is cervical cancer.