Inflammation plays a vital role in ARDS events [40], and many studies [41, 42] have shown a protective effect of hyperglycaemia against ARDS due to inhibition of the protein nuclear factor-kappa-B (NF-κB) inhibitor alpha (IκB-α) and the p56 subunit and the impairment of NF-κB activation in sepsis-induced ALI/ARDS; on the other hand, high glucose levels are associated with decreased neutrophil migration, decreased inflammatory factor secretion, and a reduced inflammatory response. The gene discussed is NFKB1; the disease is Sepsis.