Today, recognizing that a key hallmark feature of cancer is its general reprogramming of normal cell metabolism (Hanahan and Weinberg 2011), investigators also appreciate that the cancer regulating role of mitochondrial PRODH must be understood within the full proline cycle, wherein the balance between proline biosynthesis (from glutamate and ornithine via P5C reduction by PYCR1) and proline catabolism (via PRODH) differentially determines cancer cell growth, death, or senescence (Phang et al. 2012; Tanner et al. 2018). This evidence concerns the gene PYCR1 and cancer.