SMARCA4 and cancer: 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.