Recent studies show that cytidine deamination is an important feature of the mutational landscape in breast (Alexandrov et al., 2013; Burns et al., 2013a; Nik-Zainal et al., 2012), ovarian (Leonard et al., 2013), lung (de Bruin et al., 2014), and other cancers (Burns et al., 2013b; Roberts et al., 2013), with high-level expression of A3B, and experimental studies indicate that A3B may be a key driver of such mutational signatures (Burns et al., 2013a; Taylor et al., 2013). The gene discussed is APOBEC3B; the disease is cancer.