Moreover, blocking αVβ3 and αVβ5 integrins has been consistently shown to be an effective strategy for enhancing the efficacy of therapeutic agents in glioma cells.78 In some cases, simple αV knockdown can activate alternative pro-survival pathways, such as EGFR-mediated Akt signaling, to overcome this blockade.11 Since NDs preferentially bound to the most abundant integrins, whereas NDMs exhibited affinity for a broader spectrum, including all tested β subunits, they may represent more versatile vectors for integrin-targeted therapeutic approaches. Here, AKT1 is linked to glioma.