Although it may be unlikely that a single mechanism would explain every instance of A3-mediated mutations in cancers, we report here that elevated expression of the bifunctional glycosylase, NEIL2 (Figure 2A), sensitizes Hs578T breast cancer cells to two A3B-mediated effects, repair-induced mutations (Figure 2B–F) and DNA damage revealed by γH2AX foci (Burns et al., 2013a; Landry et al., 2011) (Figure 3). This evidence concerns the gene NEIL2 and cancer.