Adipose tissue has endocrine functions and promotes a cascade of pro-inflammatory cytokines and adipokines, including leptin, which may be a key factor in the pathology of asthma [27,37,38]; this is because the adipokine may induce changes in the mechanics and functions of the lungs via bronchial inflammation on admission, compared to the stable phase of the disease [42,43,44], mainly due to the accumulation of leptin-producing monocytes in the airway [45]. The gene discussed is LEP; the disease is asthma.