FIS1 and acute myeloid leukemia: An overexpression of FIS1 was also found in AML cells while FIS1 depletion impairs mitophagy, weakening the self-renewal capacity of LSCs and determining the induction of myeloid differentiation by GSK3 inactivation (glycogen synthase kinase 3), thus indicating mitophagy as being a regulatory mechanism for the progression of AML [96].