Our study reveals that concomitant loss of SMARCA4/2, but not SMARCA4 inactivation alone, strongly downregulates GLUT1 expression resulting in repressed glucose uptake and glycolysis; consequently, SMARCA4/2-deficient cancer cells elevate SLC38A2, likely acquired during tumor development, to increase import of glutamine as an alternative oxidative fuel, leading to their addiction to glutamine metabolism and OXPHOS. Here, SLC38A2 is linked to neoplasm.