For instance, how does TIM-3 affect the function of other immune cells, are there any other links between TIM-3 overexpression on different immune cells and different aspects of prognosis (i.e., resistance to different therapies, AML relapse, overall survival, refractory AML), are there mechanisms underlying upregulation of TIM-3 on LSCs, and how overexpression changes different aspects of function and stability of LSCs? This evidence concerns the gene HAVCR2 and acute myeloid leukemia.