CD8A and neoplasm: (47) confirmed that the inhibition of cholesteryl esterification by gene knockout or ACAT1 inhibitor significantly increased the production of CD3-TCR (T-cell receptor) clusters, effective immune synapses in the T-cell membrane, the proliferation of CD8+ tumor infiltrating lymphocyte cells (TILs), and the production of cytolytic granules, cytokines, and their cytotoxic anti-tumor effects; it finally prolonged the inhibition of tumor growth and survival time of mice (47).