Additional pathogenic variants in tumour suppressor genes or DNA repair genes, as well as upregulation of genes that have a synergistic effect in oncogenesis may also contribute to disease progression, with mutations in tumour protein 53 (TP53), cluster of differentiation 117 (KIT), mutS homologue 6 (MSH6), mutL homologue 1 (MLH1), ataxia-telangiectasia mutated (ATM), von Hippel-Lindau (VHL), phosphatase and tensin homolog (PTEN), cyclin dependent kinase 2A (CDKN2A) and serine/threonine kinase 11 (STK11) seen in RET or RAS mutant tumours [16,29]. The gene discussed is TP53; the disease is neoplasm.