Model of the role of MALT1 and API2-MALT1 in the NF-κB activation pathway leading to MALT lymphoma.H pylori infection induces a chronic T-cell-dependent immune reaction leading to CD40/CD40L interaction. Stimulation of B cells through CD40 activates IKK and NF-κB via a complex containing MALT1, BCL10, and CARMA. Overexpression of MALT1 or expression of API2-MALT1 as a consequence of chromosomal translocations [t(11;18)(q21;q21) or t(14;18)(q32; q21)] results in elevated constitutive and CD40-stimulated IKK activity, increasing transcription of NF-κB target genes and favoring survival and proliferation. In cases with t(11;18)(q21;q21), API2-MALT feeds back positively to sustain high constitutive NF-κB activity and reduce dependence on H pylori infection.