Healthy corneas are clear and lack blood vessels, but injuries like alkali burns can trigger neovascularization. This serious complication reduces the patient’s vision and is the leading cause of failure in corneal transplants. Previous studies have suggested that AIP1 (Apoptosis signal-regulating kinase 1-interacting protein) is involved in inflammatory neovascularization induction and that NOX4 (NADPH oxidase 4) is activated by alkali burns. NOX4 can produce reactive oxygen species (ROS) which unbalance the expression of the inflammation-related proteins NLRP3 and NLRP6 (NLR family pyrin domain containing 3 and 6). Researchers recently used a mouse model to examine how AIP1 and NOX4 are related to NLRP3/NLRP6 after corneal alkali burns. Corneal alkali burns decreased AIP1 expression and increased the expression of two pro-angiogenic proteins, clv-IL-1β (cleaved interleukin-1β) and VEGFa (vascular endothelial growth factor A). After a burn injury, AIP1 knockout mice had higher expression of NOX4 and more unbalanced NLRP3/NLRP6 than control mice. Conversely, overexpressing AIP1 reversed the burn-related impacts on NOX4 and NLRP3/NLRP6. Administering the NOX4 inhibitor GLX351322 in eye drops had a similar impact on burn-related changes. Specifically, GLX351322 reversed the imbalance in NLRP3/NLRP6, reduced ROS levels, and reduced clv-IL-1β and VEGFa expression. These findings suggest that AIP1 and NOX4 regulate corneal neovascularization after alkali burn injury and that they represent potential therapeutic targets.