MALT1 is a dual regulator of nuclear factor-κB (NF-κB) signalling: it functions as a scaffold to promote IκB kinase (IKK)-dependent activation of the canonical NF-κB pathway and proteolytically degrades several NF-κB-related factors, including the non-canonical NF-κB subunit RELB. Now, Brüstle et al. report a central role for MALT1 in the effector function of T helper 17 (TH17) cells. MALT1-deficient mice were resistant to the induction of experimental autoimmune encephalomyelitis, despite infiltration of the brain by activated T cells after immunization. Moreover, MALT1-deficient TH17 cells lacked pathogenicity and failed to produce the cytokines IL-17 and GM-CSF. Further analyses suggested that IKK activation and RELB degradation by MALT1 are two independent events that are required for the differentiation of TH17 but not TH1 cells. This function of MALT1 in T helper cell plasticity could be therapeutically targeted in autoimmune disorders.