To investigate whether ATR inhibition increases the dependence of T-ALL cells on dCK activity at the G1/S transition, CEM cells were synchronized in G1 using Palbociclib, a CDK4/6 inhibitor36, 37, and then released into media containing VE-822 and/or DI-82, a high-affinity dCK inhibitor (dCKi) developed by our group38. The gene discussed is DCK; the disease is acute lymphoblastic leukemia.