Together, results from Figures 2(a)–2(j) demonstrate that targeting E2/ERβ signaling via (i) antiestrogens to suppress E2-activated ERβ or (ii) knocking down ERβ by shRNA to suppress the ERβ all led to increasing oxidative stress-induced cell injury in human renal epithelial cells (with 0.75 mM oxalate treatment), suggesting that activation of ERβ functions may protect renal tubular cells against oxidative stress-induced renal injury in patients with hyperoxaluria. This evidence concerns the gene ESR2 and Hyperoxaluria.