ALK and inflammatory myofibroblastic tumor: This inherent machinery keeps the protein within the cell, so it is physically impossible for Augα to exert any influence on the activation of the ALK fusion protein [34] A variety of fusion ALK proteins have been reported in numerous cancers, including NSCLC, IMT, and ALCL, with fusions developing almost exclusively on the common breakpoint in exon 20 [32,35].