In our L-NAME animal model, the significant reduction of PPARα and PPARγ expression found in corneal layers, together with overexpression of well-known proinflammatory biomarkers of corneal diseases (i.e., TNF-α, COX-2, IL-1β, and IL-6 [22]) and downregulation of the anti-inflammatory cytokine IL-10, suggests that, besides the NADPH oxidase family, PPAR-related pathways might be preferential targets in the inflammatory and fibrotic processes that take place in the cornea of hypertensive animals. This evidence concerns the gene TNF and corneal disorder.