A mutation in class III receptor tyrosine kinase that is involved in the regulation of apoptosis, proliferation, and differentiation of hematopoietic cells may result in constitutive autophosphorylation of the immature form of the FLT3 receptor, resulting in strong factor-independent activation of STAT5 [21], which was previously described in acute myeloid leukemia (AML) [22,23]. Here, NTRK1 is linked to acute myeloid leukemia.