Bolstering this function of CEACAM1, defective hepatic insulin clearance and subsequently, chronic hyperinsulinemia develops in mice with global null mutation (Cc1−/−) or with liver-specific overexpression of the dominant-negative phosphorylation-defective inactive isoform of Ceacam1 (L-SACC1) (5–7). This evidence concerns the gene INS and hyperinsulinism.