Possible genetic pathways include specific translocations (for example, anaplastic lymphoma kinase [ALK] fusion in inflammatory myofibroblastic tumors), gene amplifications (for example, the amplification of MYC in radiation-induced angiosarcomas), oncogenic mutations (for example, activating mutations in the KIT receptor), and complex genomic rearrangements (vast majority of STS) [127]. Here, MYC is linked to inflammatory myofibroblastic tumor.