Since expression of a constitutive mutant of NFAT1 that mimics NFAT1 dephosphorylated, active state restores the survival and proliferation properties of calcineurin-deficient leukemic cells, our results highlight the central function of NFAT downstream of calcineurin activation in T-ALL. The gene discussed is NFATC2; the disease is acute lymphoblastic leukemia.