In this study, we show that glucose deprivation leads to robust upregulation of the expression of MT-CO2, a mitochondrial genome-encoded protein essential in the complex IV of the respiratory chain, which bridges Ras signaling to epigenetic upregulation of JUN gene transcription via activation of the FAD-LSD1-H3K9me2 axis, consequently resulting in elevated GLS1 expression, glutaminolysis, and tumor cell survival. The gene discussed is KDM1A; the disease is neoplasm.