Analyses of colorectal adenocarcinoma cell lines through the DepMap database showed that colorectal adenocarcinoma cells with KRAS mutants had a lower expression of GCLM (Figure 4d), and those with wild-type TP53 tended to have a higher expression of ACO1 (Figure 4e), implying that colorectal adenocarcinoma cells with KRAS mutations might have a lower glutathione production and thus limit antioxidative capacity, and that with wild-type TP53 tended to increase cellular redox-active iron levels to promote ferroptosis. This evidence concerns the gene ACO1 and colorectal adenocarcinoma.