The researchers noted that such imatinib-resistant mutations tend to destabilize the Src-like conformation of Abl more than the active or imatinib-bound conformations of Abl, suggesting that this conformation does indeed play a role in whether imatinib is effective in blocking the activity of Abl in CML cells. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.