In this issue of the journal, Belhaj and colleagues (pp. 584-595) evaluated the effects of his CKD (tacrolimus) preconditioning in a randomized experimental porcine model of brain death-induced lung injury. Researchers administered intravenous tacrolimus (n=8) or placebo (n=9) before infusing autologous blood to induce brain death. They measured hemodynamic changes up to 7 hours after brain death and analyzed histological features of post-euthanasia lung tissue. The authors observed that tacrolimus pretreatment was associated with beneficial hemodynamic effects and reversed many other detrimental effects of brain death. (i.e., prevented a decline in the ratio of PaO2 to FiO2), decreased circulating inflammatory markers (i.e., IL-6 to IL-10 ratio, IL-1β ratio), and improved pulmonary endothelium integrity. improved. (ie, B. vascular cell adhesion molecule)-1, a glycocalyx-derived molecule) and lung histology (ie, decreased inflammatory and apoptotic cells). Despite these encouraging results, there was no difference in lung injury scores (ie, cellular infiltration, edema, hemorrhage, and a composite marker of airway epithelial damage). The authors speculate that tacrolimus therapy did not completely eliminate the effects of systemic inflammation on donor lungs, highlighting the potential of combination therapy.