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In the 15 years since transcription factor mutation, and subsequently dosage alterations, were shown to account for a proportion of Axenfeld–Rieger syndrome cases, novel phenotypes continue to be defined. As illustrated by the spectrum of FOXC1-attributable CNS anomalies (1, 2), these are frequently present in a subset of cases and only identified by meticulous phenotyping. Our original article in PNAS (3) demonstrated that a proportion of patients with a mutation or altered FOXC1 gene dosage exhibited corneal angiogenesis, confirming our extensive data from multiple murine mutants regarding Foxc1’s role in maintaining corneal avascularity. …

Reply to Chakrabarti et al.: Corneal angiogenesis in patients with null FOXC1 variants