Taken together, these findings support the existence of a complex biologic loop in SSc, in which the TGF-β1 rich microenvironment, the up-regulated glutamine metabolism, the ehnahced glycolysis, and the fatty acid dysregulation, could all contribute to both inflammasome activation with IL-1β release and myofibroblasts differentiation, thus possibly foraging the occurrence of inflammation-driven fibrosis. This evidence concerns the gene IL1B and systemic sclerosis.