As a prime instance, results acquired from a study on an IL-38 knock-out murine model of asthma (KO) showed that severe clinical manifestations are associated with upregulation in the expression of IL-1β and IL-6 genes in the joints compared to the control ones, meanwhile, recombinant IL-38 could not be able to inhibit arthritis progression [68,69]. This evidence concerns the gene IL1F10 and arthritic joint disease.