Petljak et al. investigated the role of endogenous APOBEC3 cytidine deaminases in generating prevalent mutational signatures in human cancer genomes by deleting APOBEC3A and APOBEC3B genes in cancer cell lines naturally exhibiting APOBEC3-associated mutational signatures, demonstrating that APOBEC3A deletion significantly reduced these signatures, while the dual deletion of APOBEC3A and APOBEC3B further decreased mutation burdens without completely eliminating them. This evidence concerns the gene CDA and cancer.