Adding to this mechanistic framework, a recent integrative bioinformatic and experimental study identified FPR2 as a hub gene jointly up-regulated in atrial tissue from patients with AF and in obesity, and demonstrated that activating the ANXA1–FPR2 axis with the ANXA1 mimetic Ac2-26 reduces AF susceptibility in high fat diet obese mice by alleviating atrial lipotoxic stress via AMPK signaling [127]. The gene discussed is ANXA1; the disease is obesity due to melanocortin 4 receptor deficiency.