We concluded this based on the findings that (1) TGFβ1 induced lung fibroblast differentiation through NOX4-dependent generation of ROS, (2) pharmacological or siRNA downregulation of NOX4 significantly attenuated ROS generation, MRTF-A activation, and fibroblast differentiation, (3) pharmacological inhibition or siRNA downregulation of TRPV4 significantly inhibited NOX4 expression and fibroblast differentiation, and (5) NOX4 is upregulated in fibroblasts from asthmatic subjects and airway remodeling in experimentally induced asthma, and this response is attenuated in TRPV4 KO mice. The gene discussed is TGFB1; the disease is asthma.