For instance, FLT3ITD-mutated AML cells specifically determine STAT5 activation and p27 inhibition through the binding of their tyrosines residues 589 and 591 with Src family kinases (Lck, Hck, Fyn, Fgr, Lyn), which might explain the proliferative advantage of FLT3ITD-mutated AML over FLT3TKD-mutated AML [6,7]. Here, HCK is linked to acute myeloid leukemia.