Both receptors have been attributed a role in obesity: the FPR1 gene was downregulated in obese humans, and CYBB gene-coding NADPH-oxidase membrane subunit gp91phox was also downregulated in obese humans [12]; genetic or pharmacological inhibition of Fpr1 increased insulin levels and improved glucose tolerance, dependent upon glucagon-like peptide 1 [9]; the lack of ALX/FPR2 led to the development of spontaneous obesity, reduced life span, amplified leukocyte dysfunction, and facilitated profound interorgan non-resolving inflammation [13]. This evidence concerns the gene FPR1 and obesity disorder.