Given that insulin resistance and β-cell dysfunction are established factors that result in compromised cellular glucose uptake (via inhibition of GLUT4) and impaired carbohydrate catabolism (via diminished glucokinase activity) in individuals with type 2 diabetes (Ferrannini et al., 2020; Salway, 2017), it is expected to see elevated concentrations of urinary glucose and metabolites associated with gluconeogenesis, such as mannose (Ferrannini et al., 2020), in the poorly controlled type 2 diabetes cohort. The gene discussed is GCK; the disease is Insulin resistance.