ICAM1 and glioma: Our investigations also demonstrated that the proposed controller can (i) elicit specific changes in the BBB phenotype (AE-dependent increase in permeability and ICAM-1 expression) in healthy mice, (ii) enhance the delivery and penetration of anti-PD1 in GL261 gliomas, (iii) increase the interaction of macrophages with anti-PD1 in the GL261 TME without promoting global inflammation in nontumor tissue, (iv) improve the survival in GL261 tumor-bearing mice, and (v) synergize with anti-PD1 therapy to promote tissue-resident memory T cell formation.