Studies have shown that in thyroid cancer, neurofibromatosis 2/merlin inactivation enhances RAS signal transduction by promoting YAP/TEAD-driven oncogenic and wild-type transcription, leading to enhanced MAPK output and greater sensitivity to MEK inhibitors.[33,34] However, KDRS, CDKN2A, MAX, and RPS6KA4 are rarely reported to be related to the occurrence and treatment of GISTs, which requires further study. The gene discussed is MAX; the disease is thyroid cancer.