Similarly, a lack of adenylate-uridylate-rich elements (AREs) within the 3ʹ-UTR maintains IFNγ mRNA stability and enhances IFNγ protein expression in tumor-infiltrating T cells [66]; impaired aerobic glycolysis, which frequently occurs in the tumor microenvironment, leads to enhanced GAPDH binding to IFNγ AREs, thereby reducing IFNγ expression [25]. Here, GAPDH is linked to neoplasm.