Glutamine serves as a critical energy source for HFs, with its metabolism regulating HF stem cell fate reversibility and promoting regeneration signaling.[17] Specifically, the mTORC2–Akt signaling pathway governs glutamine metabolism, which is essential for HF stem cell regeneration and maintenance.[18] Diminished glutamine may disrupt this process, impairing HF regeneration and contributing to AA pathogenesis: consistent with the protective association observed in our study. This evidence concerns the gene AKT1 and hydrops fetalis.