In vivo studies conducted by Ackel et al. showed that inhibition of BCL-2 family proteins by navitoclax potentiates the response of B-cell lymphoma and MM models to distinct standard chemotherapeutic drugs and regimens such as etoposide, rituximab, bortezomib, cyclophosphamide, VAP (vincristine, adriamycin [doxorubicin], and prednisone), CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone), and R-CHOP (rituximab plus CHOP) [46]. This evidence concerns the gene DDIT3 and B-cell non-Hodgkin lymphoma.