Lin28a has been found to activate the NRF1-TFAM axis, thereby improving mitochondrial function and reducing cardiomyocyte apoptosis, further underscoring the critical role of NRF1 in HF progression (115) Recent evidence also shows that NRF1 directly activates CFLAR transcription to inhibit death receptor-mediated apoptosis in cardiomyocytes under hypoxic conditions, adding to its cardioprotective repertoire (116) (Supplementary Table S1). The gene discussed is NRF1; the disease is hydrops fetalis.