Among the ERGs, PAX3 showed the strongest correlation with the risk score and was overexpressed in glioma, where it promoted proliferation, migration, epithelial–mesenchymal transition, and resistance to vorinostat through regulation of HDAC1/2/3 targets, as confirmed by functional assays showing that PAX3 knockdown suppressed proliferation and migration, while overexpression enhanced these effects. This evidence concerns the gene PAX3 and central nervous system cancer.