IL-17A and IL-22 may also be important mediators of the association, with the former triggering an increase in pulmonary GM-CSF stimulating alveolar macrophages to kill and clear pathogens [48], and symbiotic bacteria stimulating the transfer of IL-22-producing group 3 innate lymphocytes to the lungs to exert anti-pneumonia effects [49]. The gene discussed is CSF2; the disease is susceptibility to pneumonia measurement.