To determine whether RPL29 is a functional mediator in PRMT1 regulation of LSCs in vivo, we transduced BM and spleen cells from primary WT or Prmt1 KO CML mice with pCDH‐vector or pCDH‐Rpl29 lentivirus and transplanted these cells into secondary recipient mice to induce CML (Figure6A). This evidence concerns the gene PRMT1 and chronic myelogenous leukemia, BCR-ABL1 positive.