TKI's, however, are not able to target LSCs, a rare, quiescent, self‐renewing cell population that initiates and sustains CML.6 Recently, Nieborowska‐Skorska and colleagues have reported that LSC from CML patients present high levels of ROS compared to normal primitive cells.7 This has been related to defects in mitochondria of CML cells, which cause the accumulation of ROS, driving genomic instability and acquired resistance to TKIs.7 This raises the interest in seeking targets other than Bcr‐Abl that may be able to eliminate LSC, which are not eliminated with current TKI therapies. Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.