In addition, studies have shown that the high levels of cholesterol in the tumor microenvironment in vivo can induce an increase in CD36 expression of CD8+ T cells, which leads to excessive intake of fatty acids, lipid oxidative damage, and iron death, resulting in the loss of its lethal function and inducing it to enter a state of exhaustion [69,70]. The gene discussed is CD8A; the disease is neoplasm.