Five of the proteins upregulated in lcSSc-PAH sera (FSTL3, Spondin-1, junctional adhesion molecule C (JAM-C), CCL28, and MDK) were investigated further for their individual ability to discriminate between subjects with lcSSc-PAH and lcSSc-no PAH in silico (logistic regression) based on biological relevance, their presence in different clusters and average fold change > 2 (Additional file 5: Figure S2). This evidence concerns the gene CCL28 and pulmonary arterial hypertension.