BTN3A1 and acute myeloid leukemia: On THP-1 cells [human monocytic cell line derived from acute myeloid leukemia (AML) patient], depletion of BTN3A1 inhibited the cytoplasmic nucleic acid- or virus-triggered activation of IFN-β production, suggesting that BTN3A1 may be a novel regulator of type I IFN responses (61).