To explore the molecular mechanism of activated CaMKIIγ in T-ALL leukemogenesis, we treated with the CaMK inhibitor KN93 and BBM, knocked out CaMKIIγ with CRISPR/Cas9 system, expressed full-length CaMKIIγ-FLAG and dnCaMKIIγ(T287A)-FLAG in Jurkat cells. The gene discussed is CAMK2G; the disease is acute lymphoblastic leukemia.