In addition, PLK4 overexpression not only recovered the expression of phosphorylated PI3K and Akt but also blocked the effect of Fraxetin on prostate cancer cells proliferation, apoptosis, migration, and invasion, revealing the crucial role of PLK4 in Fraxetin-mediated PI3K/Akt inactivation and prostate cancer inhibition. The gene discussed is AKT1; the disease is prostate cancer.