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. The gene discussed is GABPB1; the disease is neoplasm.