However, restoration of SMARCA4 or SMARCA2 in SMARCA4/2-deficient cells did not consistently suppress SLC38A2 expression (Supplementary Fig. 6f, g), suggesting that the elevated SLC38A2 levels in SMARCA4/2-deficient cancer cells may be an adaptation to suppressed glycolysis rather than a direct transcriptional regulation. Here, SLC38A2 is linked to cancer.