Considering that HDACi treatment results in deregulated STAT and NF-κB signaling [56]–[59] and that some lymphoma cells that are less sensitive to HDACi treatment have elevated levels of JAK/STAT activity [60], it is not surprising that an HDACi-sensitive cell line (SUDHL4) might up-regulate expression of any number of the anti-apoptotic proteins BCL-XL, BCL-2, and/or MCL-1 in response to prolonged and repetitive exposure to HDACi treatment. The gene discussed is BCL2; the disease is lymphoma.