When we learned about the Pentose Phosphate Pathway (PPP), I found it really interesting how it connects to some genetic disorders, especially favism, which is caused by G6PD deficiency. The PPP doesn’t produce ATP like other pathways we’ve discussed, but it generates NADPH, which helps protect red blood cells from oxidative damage. Since red blood cells don’t have mitochondria, they rely completely on this pathway to stay healthy. If the enzyme G6PD doesn’t work properly, the cells can’t make enough NADPH, and this can lead to hemolysis when someone eats certain foods like fava beans or takes specific medications. This topic caught my attention because I had an internship in the hospital in the newborn genetic disorder department. I noticed that compared to other genetic conditions, many newborns tested positive for G6PD deficiency. I already knew some basics about enzyme deficiencies, but I didn’t really understand how pathways like glycolysis and the PPP are linked in red blood cells. After learning deeply about enzyme regulation and how glucose can follow different pathways depending on the cell’s needs in our class, I gained a comprehensive understanding of why a G6PD deficiency can cause such problems. It showed how even one missing enzyme can disturb the balance between energy production and protection against oxidative stress. Although it was only one part of the knowledge in the class, it made me think more about how small changes in metabolism can lead to visible health problems, and how understanding these pathways can help in diagnosing and managing genetic disorders like favism.