To the Editor: Resolution of inflammation has long been considered to be a passive process that ensues in an inflammatory response following the dilution of proinflammatory cues. However, this paradigm is shifting as it is becoming increasingly evident that resolution is an active reaction that uses a complex molecular machinery that orderly terminates inflammation. Among the multiple mechanisms involved, specialized proresolving lipid mediators (SPMs) such as resolvins, protectins, and lipoxins have taken center stage.1 These are derived from ω3 and ω6 polyunsaturated fatty acids through complex intracellular and transcellular biosynthetic pathways, and promote resolution of inflammation by their manifold and concerted functions inhibiting leukocyte trafficking, dampening proinflammatory signaling, inducing apoptosis, and promoting anti-inflammatory M2-like macrophage phenotypes, efferocytosis, and tissue restitution.1