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. Here, ATM is linked to neoplasm.