Exogenous expression of ALFA-PRPS2 or either of the superactive ALFA-PRPS1 D52H/H193L mutants was sufficient to rescue the viability (Fig. 3I, Supplementary Fig. 3C) and restore the levels of AlamarBlue reduction (Fig. 3J, Supplementary Fig. 3D) and mitochondrial ROS accumulation (Fig. 3K, Supplementary Fig. 3E–F) of PRPS2 KO lymphoma cells, whereas exogenous expression of ALFA-PRPS1, hypomorphic ALFA-PRPS1 A87T or catalytically inactive ALFA-PRPS2 E39A did not. The gene discussed is PRPS1; the disease is lymphoma.