New treatments are now moving toward targeting the upstream pathways of asthma pathogenesis, coordinated by innate cytokines such as alarmins. These key proinflammatory mediators orchestrate the activation of complex cellular networks including both innate and adaptive immune responses. Alarmins include thymic stromal lymphopoietin (TSLP), interleukin-25 (IL-25), and interleukin-33 (IL-33), which are released from injured airway epithelial cells. TSLP and the other alarmins are suitable targets of biological therapies which are effective for add-on treatment of type 2 asthma. Moreover, anti-alarmin monoclonal antibodies can be also beneficial for patients with T2-low, poorly controlled severe asthma.