Notably, cluster 1 also displayed a signature characteristic of a potentially pro-fibrotic monocyte-derived population in IPF lungs (TREM2, MERTK, ATP6V0D2, CTSK, COL4A2, MMP7, MMP9) paired with a shift in metabolic function (FABP5, LPL and LIPA increases). This evidence concerns the gene LIPA and idiopathic pulmonary fibrosis.