We observed that exogenous overexpression of PRPS2 and the superactive PRPS1 D52H and H193L mutants largely, if not completely, re-sensitized PRPS2 KO lymphoma cells to treatment with auranofin (Supplementary Fig. 5A), carmustine (Supplementary Fig. 5B) and G6PDi-1 (Supplementary Fig. 5C), while exogenous overexpression of PRPS1, hypomorphic PRPS1 A87T and catalytically inactive PRPS2 E39A failed to do so. The gene discussed is PRPS2; the disease is lymphoma.