In this scenario, artificially inverting the proportionality of GOLPH3 with respect to the kinase caused a partial rescue of the effects of PKD2 on cell growth, indicating that (i) PKD2 is an upstream effector of GOLPH3 protein in regulating AKT activity; (ii) PKD2 could increase the level of GOLPH3 by modulating the PI3K-AKT signaling pathway in vitro; and (iii) the PKD2-GOLPH3-AKT signaling pathway might be a potential glioma therapeutic target [64]. This evidence concerns the gene GOLPH3 and central nervous system cancer.