This enhancement in stiffness may be associated with alterations in the cytoskeleton induced by changes in cellular actin levels.[27] Collectively, the increased contractility and stiffness implied that Chi3L1 promoted the differentiation of SSc DFs into myofibroblasts.[28] The qPCR assay further confirmed the rChi3L1‐induced upregulation of the expression of genes encoding ECM components (Col1A1, collagen type III, Col3A1 and fibronectin, FN1), myofibroblast marker molecules (α‐SMA and Postn) and fibrosis‐associated enzymes (tissue inhibitors of metalloproteinase 1, Timp1) (Figure 3F). This evidence concerns the gene ACTA1 and systemic sclerosis.