This constitutively active receptor expression led to lung and skin fibrosis.[13] Likewise, fibrosis was seen in mice in which connective tissue growth factor (CTGF) had been activated using transgenic overexpression.[14] Mice with postnatal deletion of type 2 TGFbeta receptor show no lung fibrosis in response to bleomycin and highlight the importance of resident lung fibroblasts in coordinating the fibrotic mechanisms in this experimental model.[15]. The gene discussed is CCN2; the disease is pulmonary fibrosis.