Interestingly, although fibroblasts isolated from patients with idiopathic pulmonary fibrosis (IPL) constitutively expressed all NOS isoforms [49], relaxin was found to inhibit lung myofibroblast contractility via a iNOS-NO-cGMP and cGMP-dependent protein kinase G-mediated pathway; again confirming the central role that NO and cGMP play in facilitating the matrix remodelling actions of relaxin, but suggesting that the NOS isoform that is involved in relaxin's actions is perhaps dependent on the specific action being executed by the hormone. The gene discussed is NOS1; the disease is pulmonary fibrosis.