NDUFS4 and columnar cell hyperplasia of the breast: In a retinal ganglion cell-specific Ndufs4 knockout model of Leber hereditary optic neuropathy, CCH evidently acted upstream of neuroinflammation, since 11% oxygen commenced at weaning led to preservation of retinal ganglion cells and decreased axonal degeneration up to at least 90 days, but did not attenuate the microglial activation that accompanied cell death (9).