Our results were consistent with previous studies, in which Gu et al. showed that FOXD2-AS1 deficiency can hinder cell proliferation and TMZ resistance and promote apoptosis in TMZ-resistant glioma cells by up-regulating miR-98-5p and decreasing CPEB4 [41], and we revealed that MSC-AS1 knockdown could impede cell proliferation, viability, and TMZ resistance and facilitate apoptosis by increasing miR-373-3p and reducing CPEB4 in vitro and in vivo through activating PI3K/Akt pathway. The gene discussed is AKT1; the disease is central nervous system cancer.