In addition to affecting NMDARs, Ca2+ entry via TRPV4 also stimulated the production of ROS and nitric oxide (NO), downregulated p‐Akt, and upregulated p‐ERK, thus exacerbating neuronal injury post‐stroke (Bubolz et al., 2012; Donko et al., 2010; Jie et al., 2016). Here, TRPV4 is linked to Stroke.