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This study, published in Theranostics, complements a related paper in Nature Communications in which the same collaborative team enhanced the VS immune microenvironment through the use of anti-VEGF therapy, resulting in lymphocyte infiltration and improved responses when combined with checkpoint inhibitors

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We further explored the mechanism of HBc degradation and found that the colchicine‐induced reduction in HBc expression was markedly blocked by the autophagy inhibitors 3-MA, CQ, and especially BafA1 but not by MG132, which is a proteasome inhibitor (Fig