A premature shutoff of Bco1 expression by ISX would put the organism at risk of systemic vitamin A deficiency (VAD), and an uncontrolled BCO1 activity would result in hypervitaminosis A. Both scenarios are detrimental and can impair vitamin A-dependent processes in vision, embryonic development, immunity, and metabolism (8, 20, 21, 22). The gene discussed is BCO1; the disease is hypervitaminosis A.