The scenario shown here is therefore opposite to that we previously outlined in normoxic conditions, where lactate was found to act as a powerful surrogate of glucose to prevent the suppression of BCR/Ablprotein expression and signaling and to maintain BCR/Abl‐dependent CML stem/progenitor cell potential [13]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.