The results here with elevated DNA damage (g-H2AX staining) in human A3A expressing murine hepatocytes, a requirement for the catalytic glutamate E72 in tumor formation, and the additional dependency on DNA deamination activity indicated by the A3A separation-of-function quadruple mutant GAAA combine to demonstrate that DNA editing is the major activity required for tumor formation. The gene discussed is H2AX; the disease is neoplasm.