For example, the pan‐HDACi SAHA (vorinostat) potentiated the therapeutic efficacy of the dual BCL‐2/BCL‐xL inhibitor ABT‐737 (a predecessor to venetoclax) to human leukemia and myeloma cells, partially through the upregulation of the pro‐death BCL‐2 protein BIM (Chen et al. 2009). The gene discussed is BCL2; the disease is plasma cell myeloma.