Furthermore, an abnormal pro-fibrotic Th2- polarized T cell response has been proposed to mediate tissue damage and fibrosis in SSc-ILD as Th2 cytokines lead to the activation of alternative inflammatory pathways and to the transcription of transforming growth factor (TGF)-β, involved in induction and progression of fibrosis [8,9]. The gene discussed is TGFB1; the disease is systemic sclerosis.