In T2-high and T2-low asthma, several environmental (e.g., respiratory viruses, bacteria, fungi and cigarette smoke) and endogenous stimuli (e.g., cytokines and chemokines) can induce the release of epithelium-derived alarmins (i.e., thymic stromal lymphopoietin (TSLP), IL-33, and IL-25), which activate both innate and adaptive immune cells [4,7]. This evidence concerns the gene TSLP and asthma.