Many studies have addressed the clinical relevance of mutations in human CUBAM, and recently it has been shown that individuals with Imerslund-Gräsbeck syndrome (I-GS), who have CUBN mutations that affect the C-terminal half of the protein, exhibit isolated proteinuria that has been interpreted as being due to defects restricted to albumin reabsorption by proximal tubular cells (Bedin et al., 2020). The gene discussed is CUBN; the disease is Gräsbeck-Imerslund disease.