Although there are likely important differences between mouse 12/15-LO and human 15-LO-1 in the context of different inflammatory settings and in their ability to mediate the production of proresolving metabolites, this study suggests that the counterregulation of 15-LO-1 by IL-13 and IFN-γ may represent an important mechanism by which IL-13 and IFN-γ mediate their opposing effects on the severity of airway inflammation in asthma. The gene discussed is IFNG; the disease is asthma.