STING1 and hydrops fetalis: Remarkably, mice deficient in STING exhibited improved cardiac function, with alleviated cardiac dysfunction and fibrosis, highlighting a direct role of cGAS-STING pathway in HF pathogenesis.373 Strikingly, Luo et al. found that doxorubicin-induced cardiac endothelial dysfunction via the cGAS-STING pathway modulated NAD homeostasis and mitochondrial bioenergetics in cardiomyocytes,374 indicating an intricate role of the cGAS-STING pathway in cell-cell crosstalk.