Furthermore, a study of serum and tissue samples from atrial fibrillation patients confirmed that elevated TREM-1 expression levels were positively correlated with inflammatory factor concentrations, and activation of its downstream PI3 K/AKT/FoxO3a pathway was also validated in clinical tissues, revealing that this pathway may participate in maintaining a pro-inflammatory microenvironment and promoting electrophysiological instability (35, 71). The gene discussed is FOXO3; the disease is atrial fibrillation.