The molecular mechanisms underlying HGMS remain incompletely understood due to its rarity; however, emerging evidence implicates several key pathways: (1) Anaplastic lymphoma kinase (ALK) dynamics—while ALK fusions characterize inflammatory myofibroblastic tumors (IMT) (17), HGMS typically lacks rearrangements. The gene discussed is ALK; the disease is inflammatory myofibroblastic tumor.