Given the mechanistic link we have established between AR-V7 and PIP5K1α, we therefore hypothesized that AR-V7 cooperates with PIP5K1α to contribute to tumor growth, thus treatment of tumors overexpressing AR-V7 with ISA-2011B, a selective PIP5K1α inhibitor may suppress the tumor growth through blocking the deregulated AR-V7 pathways. This evidence concerns the gene PIP5K1A and neoplasm.