Neutralization of IL-33 alleviated acute lung injury in rats.22 Furthermore, as observed in mice, postseptic CD4+ T cells may contribute to secondary lung infection via STAT3-mediated IL-17 production.23 Altogether, the results suggest that determining and targeting STAT3 phosphorylation could be an advantageous approach in preventing OD and secondary infections in AP. This evidence concerns the gene STAT3 and osteochondritis dissecans.