The majority of the experimental evidence that associates the metabolism of L-proline to cancer development revolves around the two genes that catalyze the last step in L-proline biosynthesis and the first step of its catabolism, namely PYCR1 and PRODH1. A simplified view of those genes’ modus operandi in cancer would implicate proline biosynthesis by the PYCR enzymes in cancer progression and its catabolism by PRODH in the suppression of tumorigenesis. This evidence concerns the gene PRODH and cancer.