TGF-β1 has been implicated as a pivotal inducer of lung fibrosis with multiple mechanisms, including EMT transition62, –64 and is known to be increased in BALF of SSc-ILD65 with immunohistochemical evaluations indicating alveolar macrophages and type 2 AECs as main producers66 and to be increased expression of TGF‐β target genes in SSc lung.67 Similarly, the evidence of IL-6 and TNF-α, and IL-8 hyperexpression in SSc-ILD lung and their ability to induce EMT in pre-clinical models68, –70 furtherly support the pathophysiological hypothesis of an immune-induced EMT in SS-ILD. This evidence concerns the gene TGFB1 and pulmonary fibrosis.