Studies characterizing tertiary lymphoid structures forming in lungs during idiopathic/heritable pulmonary arterial hypertension demonstrated high levels of CCL20 within the ELS, and a substantial infiltration of CCR6+IL17+ T cells CCL20‐sustained.34 IL‐17, however, is not the only cytokine involved: in fact, also IL‐23 and IL‐22, respectively upstream and downstream of the Th17 signaling, promote ELN in target organs, as observed in rheumatoid synovial tissue35 and salivary glands in experimental Sjogren's syndrome.36 The gene discussed is IL17A; the disease is pulmonary arterial hypertension.