Hypercarotenemia pathogenesis involves sophisticated interactions among three key mechanistic pathways: (1) intestinal absorption via SR-B1 receptors, (2) enzymatic conversion through β-carotene oxygenase 1 and 2 (Beta-carotene oxygenase 1 (BCO1)/BCO2) systems, and (3) genetic susceptibility primarily mediated by BCO1 variants (rs6564851, rs12934922, rs7501331). The condition demonstrates remarkable clinical heterogeneity influenced by individual metabolic capacity, intestinal microbiome composition, and concurrent endocrinopathies, particularly thyroid dysfunction and diabetes mellitus. The gene discussed is BCO2; the disease is endocrine system disorder.