Up to now, genes fused with ALK in IMT demonstrated contain SEC31A, TPM3, TPM4, TFG, CLTC, FN1, CARS, LMNA and PRKAR1A. Abnormal structural recombination of the ALK gene can result in aberrant activation and expression of ALK, which induces the formation of a chimeric fusion protein, leading to the proliferation of myofibroblasts and hence promote tumorigenesis, progression and metastasis of IMT. The gene discussed is PRKAR1A; the disease is inflammatory myofibroblastic tumor.