However, the study did not evaluate how urinary anti-inflammatory/pro-inflammatory balance affected CS-AKI development as key filtered pro-inflammatory biomarkers (interleukin-1β (IL-1β) and TNFα) involved in tubular injury in vitro [14] were not meaningfully detectable in normal urine [15] since they are thought to be absorbed by the tubules [16]. The gene discussed is TNF; the disease is Cowden syndrome 1.