IGHE and asthma: In the context of asthma, it has been extensively investigated that MCs are activated through the binding of high‐affinity IgE receptor FcεRI on their surface to allergen–IgE complexes, thereby triggering the release of degranulation mediators (such as histamine, prostaglandin, leukotrienes, 5‐hydroxytryptamine, chemokines, and IL‐13), ultimately leading to the allergic asthma symptoms.