NOS2 and pulmonary fibrosis: On the other hand, although the pharmacological and genetic approaches inhibited oxidative parameters to a similar extent in a bleomycin-induced pulmonary fibrosis model, they differed in their effects on fibrosis; 1400W diminished but iNOS knock-out increased pro-fibrotic markers, suggesting that iNOS appears to be necessary for controlling the late-phase response to injury [158].