In vitro experiments further confirmed that Rg3 treatment increased ULK1 and FUNDC1 expression in oxygen-glucose deprivation/reperfusion (OGD/R)-treated rat cardiomyocytes, triggered the phosphorylation of FUNDC1 at the Ser17 site via ULK1 to activate mitophagy, and facilitated FUNDC1-LC3 interactions, which resulted in the maintenance of mitochondrial homeostasis and energy metabolism and ameliorated HF (Wang X. et al., 2023). The gene discussed is FUNDC1; the disease is hydrops fetalis.