While many studies have reported that “obesity with asthma” is more often associated with a Th2 pathway, including elevated IgE and eosinophilic inflammation, other studies documented that obesity is associated to a non-Th2 inflammatory state, triggered by adipocyte hypoxia with release of the pro-inflammatory leptin, which shifts the macrophage pool in visceral fat from M2 to M1 macrophages. This evidence concerns the gene LEP and asthma.