Well-characterized examples of such therapeutics are the newly developed and promising interventions that protect neurons against excitotoxic/ischemic damages following stroke by disrupting direct or indirect interactions between NMDARs and neuronal death signaling molecules, such as neuronal Nitric Oxide Synthase (nNOS; Aarts et al., 2002; Zhou et al., 2010), death associated protein kinase 1 (DAPK1; Tu et al., 2010; Fan et al., 2014) and PTEN (Zhang et al., 2013). This evidence concerns the gene DAPK1 and Stroke.