APOBEC3B and neoplasm: For instance, the phenomenon of extremely low viral load suggests that HPV may not be the “initiating factor” driving all tumor cell clones, but more likely acts as a “promoter” or “modifier” during the early or late stages of tumor development, potentially through mechanisms such as inducing genomic instability (e.g., via APOBEC3B activation), i.e., the “oncomodulation” hypothesis (15, 71).