Dysregulation of the CCND–CDK4/6–cyclin-dependent kinase inhibitor 2A (CDKN2A)–Rb pathway may result in abnormal cell proliferation, which is a crucial mechanism of tumorigenesis in advanced solid tumor cancers, such as isocitrate dehydrogenase wild-type glioblastoma (GBM); hormone receptor (HR)-positive breast cancer; and non-small cell lung cancer (NSCLC) (2, 3). This evidence concerns the gene IDH3A and glioblastoma.