We hypothesize that the primarily cytostatic, rather than cytotoxic, effects of β-lapachone may stem from differences in NQO1 expression between normal and tumor tissues and that β-lapachone exerts its oncostatic effects mainly through the generation of peroxides via NQO1-mediated redox cycling, which then affects the DNA damage repair mechanism rather than inducing cell death directly. The gene discussed is NQO1; the disease is neoplasm.