Such tumour-like behaviour, when considered together with reduced apoptosis and hyperplasia, is consistent with impaired function of the tumour suppressor gene and critical cell cycle checkpoint regulator, TP53. Typically, mutations in the TP53 gene, or aberrations in molecular pathways affecting p53 protein expression and regulation, lead to unchecked proliferation and tumour growth [16]. The gene discussed is TP53; the disease is neoplasm.