Both non-fibrotic controls and IPF-derived fibroblasts/myofibroblasts express LXA4 receptors that enable activation of the ALXR G-protein-coupled receptor to regress a myofibroblastic phenotype to a fibroblastic one by reducing α-SMA expression, actin stress fiber formation, and nuclear Smad2/3 levels (Roach et al., 2015). The gene discussed is FPR2; the disease is idiopathic pulmonary fibrosis.