Mechanistically different from conventional PD-L1 regulation through PD-L1/PD-1 antibodies or genetic approaches, ICG@PM@NP simulates tumor-specific immunological response pathways through direct inducing mitochondria dysfunction in a persistent manner (Figs. 3 and 6), as the activated AMPK phosphorylation can effectively inhibit PD-L1 expression. This evidence concerns the gene CD274 and neoplasm.