We first characterized the expression pattern of the CARMA-BCL10-MALT1-A20-NF-κB pathway genes and found that overexpression of CBM genes in T-ALL may cause constitutive cleavage and inactivation of A20 to enhance NF-κB signaling, contributing to the pathogenesis of T-ALL. The gene discussed is NFKB1; the disease is acute lymphoblastic leukemia.