However, our analysis of potential upstream regulators did identify one small network, controlled by the cytokine oncostatin-m (OSM), that could drive relatively high expression of P-selectin (SELP), cholesterol 24-hydroxylase (CH25H), c-c motif chemokine ligand 2 (CCL2), and angiopoietin 2 (ANGPT2) and low expression of heat shock protein family B member 3 (HSPB3) in higher severity SSc patients. The gene discussed is SELP; the disease is systemic sclerosis.