Chronic myeloid leukemia develops when a gene mutates and causes an enzyme to become hyperactive, causing blood-forming stem cells in the bone marrow to grow rapidly into abnormal cells. The enzyme, Abl-kinase, is a member of the "kinase" family of enzymes, which serve as an "on" or "off" switch for many functions in our cells. In chronic myeloid leukemia, the hyperactive Abl-kinase is targeted with drugs that bind to a specific part of the enzyme and block it, aiming to ultimately kill the fast-growing cancer cell. However, treatments are often limited by the fact that the cancer cells can adapt to resist drugs. EPFL scientists have identified an alternative part of Abl-kinase on which drugs can bind and act with a reduced risk of drug resistance. Their work is published in Nature Communications.