Just as previous work had demonstrated that kinase signaling cascades downstream of CD40 engagement signal the upregulation of anti-apoptotic proteins like BCL-XL, MCL-1 and BFL-1/A1 in B-cells (20–24), so CLL cells co-cultured with CD40L-expressing fibroblasts were found to upregulate BCL-XL, MCL-1 and BFL-1 (25)—changes that rendered these cells essentially insensitive to venetoclax. This evidence concerns the gene MCL1 and B-cell chronic lymphocytic leukemia.