CDK4 and neoplasm: GABPB1 is involved in mitochondrial biosynthesis and activates GNPDA1 expression,[30] while CDK4 regulates endoplasmic reticulum (ER) stress and cellular functions.[31] Additionally, ADNP is crucial for gene activation and promotes a specific type of immune response,[32] and APH1A is associated with ER and oxidative stress responses.[33] These findings suggest that the activation of GNPDA1 may influence the ER stress response in HNSCC and that the identified genes collaborate to enhance tumor cell survival in adverse conditions.