NFKB1 and psoriasis: Consistently with the model that considers assembly of the CBM complex as a crucial point for activation of the NF-κB pathway, two highly penetrant psoriasis-linked CARMA2sh point mutations, Gly117Ser, and Glu138Ala, abrogate CARMA2 auto-inhibition and stimulate MALT1 protease activity, causing constitutive activation of the CBM complex and aberrant NF-κB-dependent induction of downstream inflammatory genes (22, 53).