In particular, the DNA cytosine deaminase activity of APOBEC-3B was shown to be up-regulated in primary breast tumors and breast cancer cell lines (Figure 4), suggesting that APOBEC3B-catalyzed deamination provides a chronic source of DNA damage in breast cancers that could select TP53 inactivation and explain how some tumors evolve rapidly and manifest heterogeneity. The gene discussed is APOBEC3B; the disease is breast neoplasm.