There has been little direct evidence that CD5, CD6, CD19 and IL7R were involved in the development of PAH, but CD5, CD6, CD19 and IL7R were T cell and B cell surface markers, and the perivascular infiltration of T and B cells correlated with the severity of PAH through aggravating EC damage and pulmonary artery remodeling [18]. The gene discussed is CD5; the disease is pulmonary arterial hypertension.