PUS7 was also found downregulated in high-risk MDS patients, and ectopic expression of mTOG markedly potentiated self-renewal and corrected differentiation bias in HSPCs of MDS patients.84 Another study reported that knockout of DNMT2, responsible for m5C modification of tRNA-Asp, tRNA-Val, and tRNA-Gly, resulted in increased tsRNAs in the bone marrow of mice and, finally, led to HSC defects. This evidence concerns the gene PUS7 and myelodysplastic syndrome.