In further support of the above data, a recent paper by Liu et al. (65) showed that the inhibition of mucosa-associated-lymphoid-tissue lymphoma-translocation gene 1 (MALT1), a scaffold protein, which recruits the IκB kinase complex leading to release and activation of NF-κB, ameliorated clinical symptoms and histopathologic features of DSS-induced colitis through NF-κB and NLRP3 inhibition, thus interfering with both inflammasome activation steps (65, 66). The gene discussed is NFKB1; the disease is colitis.