OCRL and oculocerebrorenal syndrome: Genetic mutations in the inositol-5-phosphatase OCRL1 (oculocerebrorenal syndrome of Lowe) resulted in abnormal accumulation of PtdIns(4,5)P2 in endolysosome pathways, causing delayed endocytic recycling of receptors and impaired lysosomal–autophagic dynamics and functions [22–24].