Our observation of increased α-SMA expression in in vitro generated human primary M2 M-MΦ cultures is partly comparable to the results from Rudnik and colleagues, which showed increased α-SMA expression in CD14+ monocytes from SSc patients or healthy subjects who were stimulated with a profibrotic cytokine mixture consisting of TGF-β, IL-4, IL-10 and IL-13 (10 ng/mL each) [63]. The gene discussed is ACTA1; the disease is systemic sclerosis.