PC is the result of accumulation of somatic gene mutations such as gain-of-function mutations in proto-oncogenes (i.e., KRAS) and loss of function mutation of tumour suppressor genes (i.e., CDKN2A/p16, TP53/p53, SMAD4, BRCA2 and others). This evidence concerns the gene CDKN2A and pachyonychia congenita.