In vitro observations of neuroglioma cells revealed PCSK9 overexpression led to the inhibition of c-caspase expression and stimulation of X-linked inhibitor of apoptosis (XIAP) and phosphorylated form of Akt, also known as protein kinase B (p-Akt/PKB), and consequently caused accelerated growth and development of cancer cells, while PCSK9 siRNA inhibited neuroglioma cell proliferation [185]. This evidence concerns the gene AKT1 and cancer.