We believe that this phenomenon has prevented AKI recovery to continue so that sCr had a small but new increase at D14 and NaU remained in low levels, “artificially” increasing after furosemide administration (Figure 3(a)) but decreasing again soon after and truly recovering only when the second CRP peak and leukocytosis (the second inflammatory booster) were solved with sepsis treatment. The gene discussed is CRP; the disease is acute kidney injury.