Their strategic location, their capability to recognize and respond to HF distress signals such as MICA and selected chemokines, the excessive production of IFN-γ by ILC1lc, and their direct, pathogenic effects on human HFs ex vivo documented here, all support that these cells play a hitherto unappreciated role in early AA pathogenesis. The gene discussed is MICA; the disease is hydrops fetalis.