CXCL8 and psoriasis: Interestingly, MALT1 deficiency or chemical inhibition of its catalytic activity can block hyperactivation of the inflammatory signaling program (including the induction of TNFα, IL17C, CXCL8, and HBD2 genes), triggered by pathogenic psoriasis-related CARMA2sh mutants or by cell stimulation with the fungal cell wall component zymosan or with Staphilococcus aureus, pointing to MALT1 as a potential target for therapeutic treatment of skin disorders caused by aberrant CARMA2sh signaling (22, 50, 53, 57).