Although we found that dipeptides were able to influence nutrient signalling via the mTORC1 pathway (Supplementary Fig. 6), it has been reported that rapamycin treatment does not prolong the survival of CML-affected mice29, suggesting that mTORC1 signalling is not crucial for the maintenance of CML stem cells in vivo. Because the TGF-β–FOXO–BCL6 signalling pathway is essential for CML stem cell maintenance in vivo15, 30, 31, 32, we speculated that there might be a connection between this axis and dipeptide-mediated nutrient signalling that could promote CML stem cell activity in vivo. Here, BCL6 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.