Amplification of detrimental IL-33–mediated feed-forward loops by loss of A20 function might not be restricted to initial stages in arthritis but could also play an important role in other inflammatory conditions including psoriasis, systemic sclerosis, inflammatory bowel disease, and asthma, which have an IL-33 component and are associated with A20 or A20 binding partner (TNIP1) gene locus polymorphisms [17]–[19],[44],[45]. This evidence concerns the gene TNIP1 and systemic sclerosis.