Given that the TME and tumor immunity engage in a bidirectional [140], dynamic interplay that drives immune evasion and therapeutic resistance, these compounds have been shown to reprogram tumor‐associated macrophages (TAMs) from a protumorigenic M2 phenotype toward an antitumor M1 state, attenuate the expansion of myeloid‐derived suppressor cells (MDSCs), normalize aberrant tumor vasculature, and promote cytotoxic CD8+ T‐cell infiltration [141]. This evidence concerns the gene CD8A and neoplasm.