AP-1 complexes of the c-Jun/ATF3 type promote survival of ABC DLBCL cell lines. Constitutive B-cell receptor signaling alone or in combination with activating mutations in Toll-like receptor signaling results in nuclear accumulation of c-Jun/ATF3 complexes. Short hairpin RNA–mediated silencing of signaling molecules, such as CARMA1, MALT1, MyD88, or IRAK1, results in depletion of ATF3 in cells of the ABC subtype.