It has been previously found that STEP is increased in AD and it was reported to oppose the development and strengthening of synapses via dephosphorylating and inactivating synaptic proteins including kinases like Fyn, Pyk2, and ERK1/2 (Venkitaramani et al., 2009; Xu et al., 2012; Li et al., 2014), as well as leading to the internalization of synaptic receptor complexes like GluN1/GluN2B and GluA1/GluA2 subunits of NMDA and AMPA receptors, respectively (Snyder et al., 2005; Zhang et al., 2008; Poddar et al., 2010; Wu et al., 2011; Won et al., 2019). This evidence concerns the gene MAPK3 and Alzheimer disease.