In-frame RET gene fusions that retain the kinase domains encoded by exons 13 to 16 could lead to ligand-independent, constitutive activation of RET kinase activity, which could drive tumor initiation and growth.[3] Systemic therapies for RET fusion-positive NSCLC consist mostly of targeted therapy with RET inhibitors such as selpercatinib[4] and pralsetinib,[5] both recently approved as first-line treatment. Here, RET is linked to neoplasm.