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KC normally has its onset in adolescence, progressively worsening through the third to fourth decades of life. KC patients report significant impaired vision-related quality of life. Genetic factors play an important role in KC pathogenesis. To identify novel genes in familial KC patients, we performed whole exome and genome sequencing in a four-generation family. We identified potential variants in the\n                    <jats:italic>PPIP5K2<\/jats:italic>\n                    and\n                    <jats:italic>PCSK1<\/jats:italic>\n                    genes. Using\n                    <jats:italic>in vitro<\/jats:italic>\n                    cellular model and\n                    <jats:italic>in vivo<\/jats:italic>\n                    gene-trap mouse model, we found critical evidence to support the role of PPIP5K2 in normal corneal function and KC pathogenesis. The gene-trap mouse showed irregular corneal surfaces and pathological corneal thinning resembling KC. 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