This correspondence to Gene & Diseases calls attention to the controversy between proponents of genetic modification in carcinogenesis and supporters of non-mutational oncogenesis. Data from molecular cancer research and findings from evolutionary cancer cell biology support the latter claim and provide no rationale for the mutational origin of sporadic cancers. It is more conceivable that the general susceptibility of asymmetric cell division (ACD) phenotypes to oxygen leads to irreparable DNA defects and dysregulated defective symmetric cell division (DSCD) phenotypes, and their repair through an ancient polyploid MGRS (multinucleated giant repair structures) repair mechanism initiates oncogenesis. This is reported in detail in the following lines.