Multiple studies have demonstrated that a higher expression of GLI2 is associated with inferior survival rates in FLT3-mutant AML [35,36,48], and in a novel mouse model, HH pathway activation through the expression of the constitutively active SMO mutant SMO-M2 resulted in the transformation of a myeloproliferative disorder generated by the FLT3-ITD mutation alone into AML [35]. The gene discussed is SMO; the disease is myeloproliferative disorder.