IMT is the tumor that most frequently overexpresses ALK protein, however, in addition to no expression of skeletal muscle markers Myo-D1, Myogenin and Myogenin, genetically, IMT usually shows ALK re-arrangement with many other molecular partners including TPM3, KIF5B, CARS, and THBS1 [51]. This evidence concerns the gene MYOG and inflammatory myofibroblastic tumor.