The efficacy of fludarabine in inducing dsDNA strand breaks has been shown to be proportional to the ratio of fludarabine/dATP [63], and resistance to fludarabine in CLL has been shown to correlate with increased ATP levels induced by contact with stromal cells [59], so lowering ATP levels as a consequence of c-Myc inhibition is likely to result in heightened fludarabine effectiveness. Here, MYC is linked to B-cell chronic lymphocytic leukemia.