It is known that insertion of viral sequences may cause insertional mutagenesis in the host cell while also inducing the expression of APOBEC3 clusters through IFN signaling; further, while APOBEC3A and APOBEC3B pose mutagenic potential for host cells per se, patients presenting the APOBEC3A/B deletion are described as having a greater APOBEC3-mediated mutational burden [26,29], reasonably explaining the mechanisms by which these factors may synergize to predispose patients to early-onset BC. The gene discussed is APOBEC3A; the disease is breast cancer.