Another study showed that sorafenib, a FLT3-ITD inhibitor, suppressed the activation of checkpoint kinase Chk1 to trigger DNA-damage and augmented the apoptosis of MV4-11 cells that was induced by etoposide treatment, meanwhile inactivation of GSK3 recovered durative Chk1 activation and notably abbreviated etoposide-induced apoptosis where it seems like GSK3 played opposite roles in regulating the activation of Chk1 and apoptosis of leukemia cells [26]. The gene discussed is FLT3; the disease is leukemia.