Sorafenib dose-dependently induced the generation of ROS in tumor cells in vitro and in vivo [63], and hence it is highly possible that in FLT3-ITD/D835 double mutants, RAF/MEK/ERK signaling through ATM helps to maintain proliferation and promote DNA repair, even under situations of genotoxic stress induced by high dose sorafenib. This evidence concerns the gene FLT3 and neoplasm.