KLRK1 and hydrops fetalis: A surge of interferon (IFN)-γ, secondary to the aforementioned insults, has been proposed to elicit the collapse of HF-IP and subsequent autoimmune-response-targeting HF autoantigens best represented by the activation of autoreactive cytotoxic NKG2D+CD8+ T cells plays central roles in AA pathogenesis [1,130,131,132].