Additionally, Akt activates endothelial nitric oxide synthase (eNOS) that could be produced by endothelial cells, participates in the regulation of cell permeability,22 reflect the endothelial activity, and maintains endothelial function.23 Studies have shown that the acceleration of tumor cell proliferation caused by STC2 possibly occurs via the activation of the PI3K/AKT pathway,23 which is consistent with our result. This evidence concerns the gene STC2 and neoplasm.