Her laboratory was the first to identify a genetic defect in the gene UGT1A1 that leads to Crigler–Najjar syndrome.[1] Crigler–Najjar syndrome is a disorder that disrupts normal modification and excretion of bilirubin, leading to jaundice.[2] Owens' research group also identified that UGT enzymes must be activated before they can detoxify foreign chemicals and that in some cases suppressing these enzymes could enhance the effects of therapeutic drugs.[11] Owens' laboratory found that activity of UGT enzymes can be lessened by kinase inhibitors and that protein kinase C and tyrosine kinase enzymes can alter the enzyme specificity, likely contributing to their ability to detoxify a wide range of foreign chemicals.[4]