CHK1 expression and activity in T-ALL cells are higher than in normal cells, and the DNA replication pressure caused by oncogenes phosphorylates the Chk1 cascade pathway, and the activated Chk1 suppresses the DNA replication pressure, thereby avoiding the DNA replication pressure to activate the ATM/caspase-3 apoptosis pathway, which promotes the survival of T-ALL cells5. This evidence concerns the gene CHEK1 and acute lymphoblastic leukemia.