CD274 and neoplasm: The prodrug PHPNJ NPs achieved tumor‐specific delivery of NJ due to acid‐responsive mPEG113‐b‐P(HMA50‐r‐HEMA5) shell cracking; after glutathione‐triggered cleavage of the disulfide bond, JQ1 and NLG919 were released from the NJ, and then yielded the antitumor immune response by preventing two immune escape pathways, including PD‐L1‐mediated CTL exhaustion and IDO‐1‐triggered Trp consumption.