Preclinical observations suggested that a 4- to 13-fold higher asciminib concentration was required for adequate inhibition of BCR::ABL1T315I compared with non-mutated BCR::ABL1, and in X2101 the majority of patients with T315I-mutated CML-CP who achieved responses had received doses of ≥150 mg BID [12, 23, 26, 27]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.