[113] further expanded this framework by integrating genomic, phosphoproteomic, and metabolomic data from 99 treatment‐naïve GBM cases, identifying subtype‐specific signatures in Ras signaling (PTPN11/PLCγ1), metabolic reprogramming (e.g., IDH‐mutant 2‐hydroxyglutarate accumulation), and immune phenotypes (H2B acetylation‐driven subtypes). The gene discussed is IDH1; the disease is glioblastoma.