However, the treatment resistance and long-term toxic side effects of current therapies in a subset of patients pose the need for more targeted therapies, prompting the consideration of BET inhibition as a potential therapeutic approach [35]. Ott et al. showed JQ1 potently reduced the viability of those B-ALL cell lines with high-risk cytogenetics, particularly lines with CRLF2 rearrangements. They found JQ1 downregulated transcription of IL7R, which normally heterodimerizes with CRLF2 and signals through JAK1/2 and STAT5 pathways to promote cell proliferation. The gene discussed is CRLF2; the disease is acute lymphoblastic leukemia.