We hypothesized that there are altered FPR1/FPR2/FPR3 expressions of blood immune cells, imbalanced M1/M2 monocyte, and differential expressions of five FPR ligands, including SAA, LL37, LXA4, ANXA1, and RvD1, in the systemic inflammatory environment of COPD, opposing protective anti-inflammatory and pro-resolution pathways [4]. This evidence concerns the gene CAMP and chronic obstructive pulmonary disease.