More strikingly, addition of dimethyl α-ketoglutarate (α-KG), a cell-permeable α-KG analog, significantly suppressed apoptosis of Kelly cells induced by GLS2 knockdown (Figure 3E), suggesting that MYCN-amplified neuroblastoma cells rely on GLS2-mediated glutaminolysis to replenish TCA cycle intermediates essential for mitochondrial integrity and cell survival. Here, GLS2 is linked to neuroblastoma.