The irregularities of the mouse anterior corneal surface and localized abnormal corneal thinning in the Ppip5k2+/K^ and Ppip5k2K^/K^ mice clearly indicate the critical role of Ppip5k2 in maintaining the physiological function of the mouse cornea, consistent with the potentially important role of PPIP5K2 in the pathogenesis of KC in human patients. The gene discussed is PPIP5K2; the disease is keratoconus.