For example, a weak but persistent activation of α7* nAChRs can be achieved with low concentrations of nicotinic agonists (e.g., ∼1–6 μM 4OH-GTS-21 (i.e., 3-(4-hydroxy, 2-methoxy-benzylidene)anabaseine), a selective α7 nAChR agonist [56], [66]) and has been shown to be neuroprotective in the NGF/serum-withdrawal toxicity model in pheochromocytoma-12 cells expressing functional α7* nAChRs [22]. Here, CHRNA7 is linked to pheochromocytoma.