In the light of the above-described results, highlighting a key role of NCKX2 during cerebral ischemia, the aims of this study were: (a) to evaluate whether NCKX2 intervenes in preconditioning-elicited neuroprotection and (b) to clarify whether modifications in NCKX2 expression occurring during this neuroprotective strategy depend on AKT or on calpain-dependent post-translational pathways. This evidence concerns the gene SLC24A2 and brain ischemia.