PDE10 inhibition can increase intracellular levels of cGMP and cAMP to activate PKG and PKA signaling, respectively, although the mechanism responsible for its tumor cell growth inhibitory activity may be exclusively associated with cGMP/PKG signaling, given that cAMP PDE specific inhibitors (e.g. rolipram) or PKA activators (e.g. forskolin) do not inhibit colon tumor cell growth [12, 31-33]. This evidence concerns the gene PRKG1 and neoplasm.