In CLL cells, AR-42 can not only increase the sensitivity of CLL cells to TNF-related apoptosis inducing ligand (TRAIL) by reducing the expression of cellular FLICE (FADD-like IL-1β-converting enzyme)-like inhibitory protein (c-FLIP), but also engender dose and time-dependent acetylation of histone, thereby inducing apoptosis from dependence on caspase [109]. This evidence concerns the gene TNFSF10 and B-cell chronic lymphocytic leukemia.