Experimental studies have demonstrated that monocytic differentiation of the AML cells is associated with sensitivity to BET inhibitors; the monocytic differentiation regulators SPI1 (Spi-1 proto-oncogene), FOS (Fos proto-oncogene, AP-1 transcription factor subunit), JUNB (JunB proto-oncogene, AP-1 transcription factor subunit) and AHR (aryl hydrocarbon receptor) seem to be of particular importance for the responsiveness and show high levels in monocytic AML cells [169]. The gene discussed is JUN; the disease is acute myeloid leukemia.