FECH and cancer: This cancer specificity can be attributed to differences in the porphyrin biosynthetic pathway activity in tumors versus normal tissues [36], including (i) the lack of ferrochelatase (the enzyme responsible for the insertion of Fe into PpIX to convert it into heme) in tumors [37], (ii) the reduced availability of Fe in tumor cells [38] to catalyze the PpIX–heme conversion, and (iii) the increased activity of enzymes [39,40] (e.g., porphobilinogen deaminase) that promote PpIX synthesis in cancer cells.