In syngeneic murine breast, lung, and colorectal cancer models, HDAC inhibitor Tucidinostat polarized M2 macrophages to the M1 phenotype by activating the NF-κB signaling pathway, promoted the expression of chemoattractant CCL5 leading to the infiltration of CD8 + T cells, and decreased tumor resistance to anti-PD-L1 immunotherapy (58). The gene discussed is CD8A; the disease is neoplasm.