This notion is supported by several lines of evidence: first, pharmacologic and genetic inhibition of sEH has been shown to protect against DOX-induced nephrotoxicity [8, 9]; second, inhibition of sEH has been shown to protect against other models of nephropathy [30, 46]; third, EETs have both anti-apoptotic [47] and anti-fibrotic [48] properties in the kidney. The gene discussed is EPHX2; the disease is kidney disorder.