Additionally, we observed that Cxcr1 deficiency in Ly6C+ cDC2s facilitated the differentiation of naïve T cells into Tregs, potentially due to feedback inhibition of Th17 differentiation or a modest increase in Lif, a potent factor that promotes Treg differentiation.[27, 28] Interestingly, these activities associated with Cxcr1 deficiency were not observed in other cDC subsets, indicating that Ly6C+ cDC2s, rather than other cDC populations, exert pro‐inflammatory effects and drive the progression of ALI in a Cxcr1‐dependent manner. The gene discussed is CXCR1; the disease is acute respiratory distress syndrome.