Previous works have demonstrated a critical role of PHZ in preventing and treating MDs by directly decreasing the blood glucose level via competitive inhibition of SGLT2;35,36 however, the extremely low bioavailability of PHZ casted doubt on whether this was the only mechanism behind the therapeutic effect.10 Thus, the current work hypothesized that the gut microbiota was an alternative target responsible for the observed beneficial effects of PHZ intake. Here, SLC5A2 is linked to myelodysplastic syndrome.