Although inflammation is no longer considered the main driving force behind IPF development and progression [2, 8], this analysis showed enrichment of various immune-related pathways in IPF-ECs, including the TNF, IL-17, and JAK-STAT signaling pathways (p < 0.05) (Fig. 3a+b). The gene discussed is IL17A; the disease is idiopathic pulmonary fibrosis.