On the other hand, it is unlikely that empagliflozin treatment attenuated inflammation, a possible mechanism of AKI after MI in diabetes3, because the increases in renal mRNA levels of TNF-α, IL-1β, and IL-18 in OLETF were not suppressed by empagliflozin (Fig. 6c) as was found in our previous study using canagliflozin4. The gene discussed is TNF; the disease is acute kidney injury.