This hypothesis is based on the fact that analysis of NGS sequencing data have shown that very few genes are mutated, deleted and/or amplified at high frequencies in sporadic human cancers, those worth mentioning include the TP53 tumor suppressor and DNA damage checkpoint gene and genes that negatively regulate cell growth, such as the CDKN2A/B genes. The gene discussed is CDKN2A; the disease is neoplasm.