Intriguingly, contrary to what has been observed in the GBM model, the protease activity of MALT1 is largely dispensable for EGFR-induced NF-κB activation in lung carcinoma, since the reconstitution of MALT1-silenced cells with a protease-deficient mutant MALT1 (MALT1C464A) fully restores NF-κB signaling. Here, NFKB1 is linked to lung carcinoma.