After treatment with a PI3K inhibitor, some pathological manifestations of asthma (such as increased amounts of activated chemokines in eosinophils, bronchoalveolar lavage fluid IL-5 and IL-13, lung tissue eosinophilia, increased mucus secretion in the respiratory tract, airway hyperresponsiveness, etc.)are obviously inhibited, and PI3K/AKT signaling highly regulates asthma pathogenesis.288. The gene discussed is IL13; the disease is asthma.