In this regard, we observed a strong functional relationship between the FASN status and the mitochondrial capacity to perform oxidative phosphorylation via the ETC, thus experimentally confirming one of the predicted cancer cell dependencies that mimics the consequence of depleting FASN. Our genetic and pharmacological approaches confirm and extend some of the previous evidence suggesting a close relationship between the functional status of FASN and the rate of oxidative phosphorylation in cancer and immune cells [96, 97]. Here, FASN is linked to cancer.