A recent study using stably-transfected HEK cells overexpressing human OATP4C1 showed that OATP4C1 can mediate the uptake as well as the efflux of L-arginine (uptake KM of 48.1 μM) ADMA (uptake KM value of 232.1 μM) and homoarginine (uptake KM value of 49.9 μM) [212] (Table 5), suggesting that OATP4C1 may be involved in the excretion of uremic toxins in renal failure. The gene discussed is SLCO4C1; the disease is kidney failure.