The same research group, in a later work, specified that the cGMP-mediated inhibition of breast tumor cell growth by sulindac sulfide or known PDE5 pharmacologic inhibitors (e.g., MY5445 and tadalafil) was due to the degradation of nuclear β-catenin following its phosphorylation at the serine 33–37, or threonine 41 residues by PKG and, as a consequence, the suppression of oncogenes regulated by β-catenin, including survivin and vasodilator-stimulated phosphoprotein (VASP). Here, PRKG1 is linked to breast neoplasm.