Using a PRODH/POX-expressing DLD colorectal cancer cell model and mouse mitochondria, we demonstrate that PRODH/POX passes electrons directly to Coenzyme Q1 (CoQ1), and that acute proline treatment in PRODH/POX-expressing cells resulted in Complex I- and Complex II-independent oxidative respiration during nutrient stress conditions. This evidence concerns the gene PRODH and colorectal cancer.