ACSL4 and colonic neoplasm: CDK1 directly binds and phosphorylates the S447 site of ACSL4, promoting the ubiquitination degradation of ACSL4, while genetic and pharmacological blocking of CDK1 enhances ACSL4 activity, promoting ferroptosis of colon cancer cells and increasing their susceptibility to oxaliplatin.190 These studies suggest that promoting ferroptosis is a promising strategy to overcome drug resistance in colon cancer patients.