A1AT administration has been reported to inactivate the p21-activated kinase (PAK)/signal transducer and activator of transcription 1 (STAT1)/p38MAPK signaling pathway in trophoblasts from patients with preeclampsia [22,23], and S-nitrosylated A1AT was found to enhance the expression of inflammatory factors by activating p38MAPK and JNK [24]. The gene discussed is STAT1; the disease is preeclampsia.