Activated Src has been found to phosphorylate tau at tyrosine residues, implicating its action is tau pathology, while Src can also phosphorylate NMDA receptors, thereby controlling their expression at the postsynaptic density and implicating Src in disease pathogenesis in such disorders as AD and HD (Ali and Salter, 2001; Salter and Kalia, 2004; Scales et al., 2011). This evidence concerns the gene SRC and Huntington disease.