Along with the inability of PQ10 to increase the phosphorylation of β-catenin at pSer675, these results suggest that PKG activation may be the predominant signaling pathway to phosphorylate β-catenin in response to PQ10 treatment and to inhibit tumor cell growth, which is supported by previous reports that cAMP elevation and PKA activation do not appear to be essential for the growth inhibitory activity of PDE10 inhibitors [31-33]. The gene discussed is PRKG1; the disease is neoplasm.