This inhibitory effect is also mediated by blocking the STAT/VEGF pathway in both tumor cells and endothelial cells, leading to a decrease in phosphorylated STAT-1 and phosphorylated STAT-3, along with a downregulation of angiogenesis-promoting factors like VEGF, bFGF, iNOS, eNOS, and MMP-2 in HUVECs [55]. This evidence concerns the gene SOAT1 and neoplasm.