Studies on NHL cell lines have discovered that the expression level of BCL-XL correlated with reduced sensitivity to anti-CD79b-valine-citrulline-MMAE, with in vivo data demonstrating that inhibition of BCL-2 with ABT-263 could enhance the activity and restore tumor responsiveness to treatment with anti-CD79b-vc-MMAE[70,75]. The gene discussed is CD79B; the disease is neoplasm.