NFATC3 and Alzheimer disease: Previous work on human AD brain tissue and rodent models of AD-like pathology suggest that elevated NFAT4 signaling is attributable to increased CN levels, changes in the subcellular localization of CN, and/or to the pathologic proteolysis of CN into high activity fragments (Abdul et al., 2009; Wu et al., 2010; Furman et al., 2016; Pleiss et al., 2016; Sompol et al., 2017).