This seems to be in accord with the similar regulation taking place under neurotoxic conditions, such as under exposure to amyloid-beta or apoE4 (Cedazo-Mínguez et al., 2003), as well as in experimental diabetes, traumatic brain injury, and cerebral ischemia in rodents (Planel et al., 2007; Zhao et al., 2012; Morales-Corraliza et al., 2016; Kisoh et al., 2017; van der Harg et al., 2017), where at early stages following model induction indeed the expected decrease in GSK3β (S9) [with also an increase in GSK3β (Y216) was detected, but at latter stages the opposite effects were detected]. The gene discussed is GSK3B; the disease is brain injury.