In non-alcoholic steatohepatitis (NASH), a significant loss of glycosylation of OATP1B1 and OATP1B3 was recently reported, suggesting that the loss of glycosylation of OATP1B1 and OATP1B3 may contribute to altered drug disposition in NASH [125]. The gene discussed is SLCO1B3; the disease is metabolic dysfunction-associated steatohepatitis.