AKT1 and neoplasm: However, in this study, the expression of TNFRSF14 was positively correlated with OS in patients with endothelial cancer and we speculated that this may be due to the following reasons: (1) TNFRSF14 activation can upregulate caspase-3 expression, and thus, promote the apoptosis of tumor cells [87]; and (2) TNFRSF14 can inhibit epithelial-to-mesenchymal transition (EMT) by blocking the PI3K-AKT signaling pathway through the inhibition of AKT expression [88].