Some studies have shown that inhibiting the uptake of AA I in the kidney or enhancing the metabolism of AA I in the liver and kidney can reduce the nephrotoxicity of AA I. Baudoux et al. observed that in vitro use of probenecid, a drug for treating gout, restricted the entry of AA I into renal tubules by inhibiting organic anion transporters [41]. Here, TEAD1 is linked to gout.