PRPS1 and neoplasm: Dihydropyrimidine dehydrogenase (DPD)‐mediated conversion of 5‐FU to dihydrofluorouracil (DHFU) is the rate‐limiting step of 5‐FU catabolism in normal and tumor cells, and up to 80% of administered 5‐FU is broken down by DPD in the liver.9 Numerous studies have shown that expression levels of TS, DPD and OPRT could affect tumor cell sensitivity to 5‐FU.10, 11, 12, 13, 14 However, it remains unknown whether 5‐FU has effective role in treating ALL, and especially targeting PRPS1 mutant ALL cells.