Similarly, our previous studies indicated that a significantly greater reduction of NF-κB activity [5], neutrophil chemotaxis [6], and TREM-1 and p38 mitogen-activated protein kinase activity [7] and pulmonary endothelium leakage [8] in sepsis-induced ALI was observed in the iPSC-CM group versus the iPSCs group. The gene discussed is TREM1; the disease is acute respiratory distress syndrome.