Inhibition of N822K T>A mutation-induced constitutive c-KIT activation in AML cells triggers apoptotic and autophagic pathways leading to death

The D816V mutation of c-KIT can constitutively activate tyrosine kinase, thereby promote core binding factor acute myeloid leukemia (CBF-AML) cell proliferation and inhibit apoptosis. Previous studies have indicated similar proliferation and apoptosis between N822K and D816V mutations.