For example, if compensation for unmet dNTP demand induced by loss of p53R2 occurs predominantly by salvage enzyme compensation, deoxynucleoside analogs such as gemcitabine [3] and decitabine (DAC) [4] may be optimal for treating cancers of such cells; DAC therapy would then have the additional advantage of promoting cell cycle exit by p53-independent differentiation mechanisms [5]. The gene discussed is RRM2B; the disease is cancer.