We employed five different experimental paradigms to target phosphoinositide recycling in these tumor models: direct targeting of Cds2 using separate translation or splice blocking vivoMorpholinos (vMO)40, inhibition of inositol monophosphatase (IMPase) activity by the potent chemical inhibitor L-690,48841, inhibition of IMPase activity by lithium chloride (LiCl) treatment, and inducible, endothelial-specific genetic deletion of Cds2 in mice via the Cre/Lox system. The gene discussed is CDS2; the disease is neoplasm.