The findings that: (i) oxidative DNA damage occurs at YC:GR sites, which overlap with APOBEC3B specificity; (ii) numerous oxidation products can form at the target GR; (iii) efficient charge transfer and high mutation rates co-localize with heterochromatin; and (iv) some oxidation products of guanine are obligate mutagens during TLS, make it tempting to attribute a significant role for oxidative damage in mutations at YC:GR sites genome-wide in cancer mutagenesis. Here, APOBEC3B is linked to cancer.