Given the observation that concomitant loss of TP53 and TP73 is rather infrequent in cancer (at least in CRC and breast cancer) this also suggests that routes other than p53/p73 loss can result in lowered expression of CDKN1A and increased CDK1 activity and contribute to abnormally increased microtubule polymerization rates and CIN in human cancer (Fig. 7). The gene discussed is TP53; the disease is breast carcinoma.