In these hosts, HDL‐C might affect immune cells in the tumor microenvironment instead of directly killing tumor cells.18 In studies comparing syngeneic B16F10L tumors from mice that were either apoA‐I deficient or mice expressing human apoA‐I, the results showed that the increasing levels of apoA‐I/HDL decreased the recruitment of myeloid‐derived suppressor cells (MDSC) and promoted the accumulation of tumor‐associated macrophages (TAMs) with an M1‐like phenotype, and inhibited the accumulation of M2‐like TAMs within tumor beds.18, 19. The gene discussed is APOA1; the disease is neoplasm.