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. The gene discussed is IL33; the disease is osteochondritis dissecans.