As sympathetic nerve activity has been suggested to maintain ATMs in an anti-inflammatory state via macrophage B2AR signaling [13], and as sympathetic nerve-associated ATMs acquire greater pro-inflammatory phenotype than a general ATM population in response to high-fat feeding [9], we hypothesized that B2AR signaling in macrophages could be important to limit ATM M1 polarization and WAT inflammation in obesity. Here, ATM is linked to obesity due to melanocortin 4 receptor deficiency.