In patients with IPF, senescent cells in the lung microenvironment displaying this ROS-induced feature secrete a wide range of proinflammatory and profibrotic mediators, such as IL-1β, IL-6, plasminogen activator inhibitor-1 (PAI-1), VCAM-1, matrix metalloproteinase-2 (MMP-2), and TGF-β (Álvarez et al., 2017), which collectively function as a signaling hub that perpetuates tissue injury responses and drives fibrotic progression (Schafer et al., 2017; Waters et al., 2018). This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.