Constitutive Hh activation leads to downstream STAT5 signaling, and combined treatment with the tyrosine kinase inhibitor, sorafenib and SMO antagonist IPI-926 inhibited clonogenic AML growth and proliferation in FLT3-ITD+ AML cell lines in vitro and disease progression in vivo [109]. This evidence concerns the gene FLT3 and acute myeloid leukemia.