GPX4 and colorectal carcinoma: Similar to the data shown earlier (Fig. 3J, K), both Erastin and RSL3 significantly reduced the viability of ARID1A-KO cells compared to wild-type cells, while re-supplementation of c-MET significantly rescued RSL3/Erastin-induced cell death (Supplementary Fig. 6), suggesting that c-MET signaling is crucially involved in NRF2-GPX4 axis and ferroptosis regulation in ARID1A-deficient CRC cells.