Several signaling pathways have been reported to be involved in the pro-inflammatory phenotype of LSECs, including the downregulation of vascular endothelial growth factor-stimulated NO production (Deleve et al., 2008), NOX1 upregulation in certain liver diseases, such as NAFLD (Matsumoto et al., 2018), and decreased nitric oxide synthase 3 expression (Takada et al., 2018). Here, NOS3 is linked to metabolic dysfunction-associated steatotic liver disease.