Cough variant asthma (CVA) is a specific type of asthma in which cough is the only or main manifestation without significant wheezing, and is one of the main causes of chronic cough in children. However, there are differences in respiratory inflammation, severity of airway remodeling and respiratory reactivity between CVA and typical asthma, only in terms of severity or stage of disease progression. Due to individual differences in genetic quality and inconsistent environmental stimuli that induce airway inflammation, different organisms do not produce exactly the same response. Therefore, different organisms may have different clinical manifestations at different times and in different settings. When the airway inflammation is mild or superficial in asthma, it may not cause bronchial smooth muscle spasm or mild bronchospasm, and if the swelling of bronchial mucosa is the main cause, the clinical manifestation may be mainly chest tightness, or if the irritation is only on the surface of airway mucosa, the clinical manifestation may be only irritating dry cough. The pathogenesis of CVA may be related to the following factors: (1) genetics, environment and infection: CVA is also genetically polygenic, with a heritability of 80%, and often occurs in specific populations. Environmental pollution (e.g., passive smoking) and infections, especially viral infections, are associated with the development of CVA. (2) Immunity: TH1/TH2 imbalance, especially a decrease in TH1, can lead to the production of large amounts of inflammatory mediators, resulting in chronic airway inflammation. From the immunological point of view, CVA is a systemic metabolic disease with immune dysfunction, and airway variant inflammation is only one of the local manifestations, so attention should be paid to the adjustment of systemic immune function after the symptoms are relieved. (3) Airway neuromodulation: airway obstruction caused by neural imbalance can trigger the disease. Most current studies suggest that the pathogenesis of CVA and CA is similar, with the pathology manifesting as chronic airway inflammation and airway hyperresponsiveness dominated by eosinophils. Inflammatory marker species such as eosinophilic cationic protein (ECP), interleukins (IL-5, IL-8), tumor necrosis factor (TNF-α) and cell counts are significantly increased in sputum. The percentage of eosinophils in sputum is an important predictor of the development of CVA to CA. In addition, chronic inflammation causes damage to the bronchial epithelium and exposes the vagal nerve endings, which are tightly bound to the epithelial cells, with a lower than normal excitation threshold and increased sensitivity to various stimuli, i.e., airway hyperreactivity. Therefore, the occurrence of CVA can be triggered by every cold, environmental factors, and physicochemical stimuli. Xing Xianghui, Department of Pediatrics, Affiliated Hospital of Shandong University of Traditional Chinese Medicine