Notably, the authors discovered that NSD3-driven LUSC tumorigenesis was more sensitive to bromodomain and extra-terminal (BET) inhibitors (Fig. 1).1 This is consistent with the previous studies, in which depleting NSD3 could intensively sensitize acute myeloid leukemia cells to BET inhibitors.3 These findings offer a potential strategy for the treatment of NSD3-driven malignancies and may also expand the indication of BET inhibitors. The gene discussed is NSD3; the disease is acute myeloid leukemia.