In addition, to the existing knowledge that (myo)fibroblast-mediated ECM deposition can be induced by various cell types and cytokines—including members of the IL-1 superfamily—it is conceivable, though not yet mechanistically proven, that IL-1R1 signaling orchestrates epithelial-to-mesenchymal transition (EMT) and/or endothelial-to-mesenchymal transition (EndoMT) through the upregulation of key transcriptional regulators, thereby enabling stromal niche reprogramming and cell differentiation associated with fibrosis in PSC and IBD [99,148,229,230,231,232,233]. This evidence concerns the gene IL1B and inflammatory bowel disease.