Accordingly, the pre-treatment of NK92 cells with TGF-β impaired the formation of immunological synapses in the early phase of our co-cultures, restraining the observed BETi ability to improve target tumor cell recognition and further supporting the central role of SMAD3 inhibition in mediating BETi anti-tumor effects (Fig. 5K, Suppl. The gene discussed is TGFB1; the disease is neoplasm.