Based on these findings, we propose that a possible underlying mechanism of prednisone-dependent severe eosinophilic asthma may be airway autoimmune responses, whereby the presence of airway autoantibodies drives the TL1A–DR3 axis, subsequently activating ILC2 and leading to downstream type 2 inflammation and airway eosinophilia. The gene discussed is TNFRSF25; the disease is Increased total eosinophil count.