In other models, RvD1 contributed to the protection from the deterioration of tight junction proteins in a model of acute lung injury induced by lipopolysaccharide in mice by inducing HO-1 expression (Xie et al., 2013); increased GSH levels and HO-1 mRNA expression in carbon tetrachloride (CCl4)-induced acute liver injury model (Chen et al., 2016); and inhalation of CO accelerates inflammation resolution by inducing RvD1-dependent activation of HO-1 (Chiang et al., 2013). The gene discussed is HMOX1; the disease is injury.