MSCs overexpressing HO‐1 exhibited superior prosurvival and antiapoptotic properties and thus exerted an enhanced protective efficacy to attenuate lipopolysaccharide‐induced acute lung injury in rats.28 Transfection with HO‐1 in MSCs greatly attenuated iron overload‐induced apoptosis by inhibiting reactive oxygen species generation and IL‐10 secretion.29 Nevertheless, gene modification can affect the genome stability of MSCs. Here, IL10 is linked to injury.