Hashimoto et al. used a model of LTB4-induced mouse dermatitis to examine the relationship between glucocorticoids and lipoxin A4 receptors and found that the anti-inflammatory effects of glucocorticoids may be attributable, in part, to the upregulation of ALX/FPR2, suggesting that the lipoxin system may serve as a negative regulator for LTB4 signaling [33]. Here, FPR2 is linked to skin disorder.