Altogether with another study used insulin treatment in a cloned rat pheochromocytoma cell lines showed that increase in the p-GSK-3β (Ser9) levels agreed roughly with the repression in p-GSK-3β (Tyr216) because insulin activate Akt, an inhibitor for ERK1/2 as well as GSK-3β (Tyr216) (Krishnankutty et al. 2017). The gene discussed is AKT1; the disease is hereditary pheochromocytoma-paraganglioma.