Currently [63], the diagnosis of GS includes the following: isolated, asymptomatic unconjugated hyperbilirubinemia (17–70 μmol/L [1–4 mg/dL]); liver enzyme activities (ALT, AST, ALP, GGT) within physiological range; absence of overt signs of hemolysis (reticulocyte count <1.5%, negative Coombs test); and genetic testing reserved for individuals with higher serum bilirubin concentrations to differentiate GS from Crigler–Najjar syndrome type 2 or when considering treatment with medications that affect UGT1A1 activity. The gene discussed is UGT1A1; the disease is Hyperbilirubinemia.