AKR1C3 and neoplasm: After rapid hydrolysis of PR-104 to PR-104A by systemic phosphatases, PR-104A becomes activated by NADPH-cytochrome P450 oxidoreductases and other one-electron reductases in hypoxia, or under oxic conditions by AKR1C3, to reactive nitrogen mustards (hydroxylamine PR-104H and amine PR-104M) that crosslink DNA causing tumour cytotoxicity[3-6].