A report showed that OAT3 deficiency damaged the glucosuric effect of empagliflozin [122], indicating that the decreased expression of renal OAT3 by diabetes may attenuate the glucosuric effect of empagliflozin, which may also explain the clinic finding that compared with normal renal function and normal-to-mildly reduced renal function, diabetic patients with mild-to-moderately reduced renal function showed the lowest lowering glucose effect of luseogliflozin [123]. The gene discussed is SLC22A8; the disease is diabetes mellitus.