In contrast to other TKIs, asciminib allosterically binds to the myristoyl pocket of the BCR-ABL1 protein, locking it into an inactive conformation without blocking the kinase ATP-binding site.15,28,29 This unique mechanism of action allows for targeting of both native and mutated BCR-ABL1 proteins, including those with the BCR-ABLT315I mutation.29 Furthermore, preclinical data showed that asciminib inhibits ABL1 tyrosine kinase in vitro, inhibits cell growth and proliferation in BCR-ABL1 expressing cells, and inhibits tumor growth in mouse xenograft BCR-ABL1 expressing CML.30 Here, ABL1 is linked to neoplasm.