In addition, Chen et al. demonstrated that miR-199a-3pexpression was decreased in ALI due to the binding of C-terminal-binding protein 2–histone deacetylase 1–FOXP3 transcriptional complex (CHFTC) to its promoter, resulting in elevation of the expression level of nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing protein 1 (NLRP1), which activates the release of inflammatory markers (IL-1β and IL-18), exacerbating the inflammatory response in ALI [37]. The gene discussed is FOXP3; the disease is acute respiratory distress syndrome.