These findings, in association with the reported strong expression of ST2L in endothelial cells, inflammatory/immune cells, and myofibroblasts in early stage SSc, suggested a role of IL-33 in the active derangement of the microcirculation, as well in other pathogenetic mechanisms of SSc, such as immune abnormalities and fibrosis [109]. This evidence concerns the gene IL1RL1 and systemic sclerosis.