Research using FLT3 inhibitor-resistant leukemia cell lines generated through prolonged cocultures with FLT3 inhibitors has revealed that FLT3 inhibitor-resistant cells most frequently become FLT3 independent because of the activation of parallel signaling pathways that provide compensatory survival/proliferation signals when FLT3 is inhibited [93]. The gene discussed is FLT3; the disease is leukemia.