However, the majority of these tumours exhibit loss-of-function point mutations or copy number deletions of the TP53 and CDKN2A tumour suppressor genes and all but one of these tumours exhibit multiple copy number gains or amplifications of genes involved in the RAS-RAF-MEK-MAPK signalling cascade, as well as copy number losses of the NF1 tumour suppressor gene that negatively regulates signalling by this cascade. The gene discussed is TP53; the disease is neoplasm.