However, in B‐ALL, activating RAS mutations, namely in NRAS and KRAS, are frequently found upon relapse and are known to confer resistance to chemotherapy1, 3, 4, 5 by aberrant activation of the downstream signalling cascade via RAF/MEK/ERK with a connection to PI3K/AKT/mTOR signalling.6, 7, 8. The gene discussed is AKT1; the disease is acute lymphoblastic leukemia.