It was previously reported that nuclear PKM2 could phosphorylate histone H3, triggering consequent EGFR signaling for tumorigenesis and forming a positive feedback loop to enhance expression of glycolytic enzymes as well as the cancer promoting factors Oct4, HIF1α, and Signal Transducer and Activator of Transcription3 (STAT3) [62], indicating that the nucleus translocated PKM2 may act more oncogenically than its cytoplasmic counterpart. The gene discussed is EGFR; the disease is cancer.