Fig. 6From: Chronic myeloid leukemia: cytogenetics and molecular biology’s part in the comprehension and management of the pathology and treatment evolutionATP binding is essential for BCR-ABL to phosphorylate substrates (with a release of ADP) and then activate the signaling cascade which promotes cell survival and proliferation leading to CML. TKIs competitively bind to ATP-binding sites, thereby blocking signal transduction. Type 1 inhibitors bind to the active conformation of the kinase, while type 2 inhibitors target the inactive conformation of the kinase domain (Created on BioRender)Back to article page