Given the relevance of AQP9 in facilitating the entry of glycerol, the carbon backbone of TAG, into hepatocytes, it is reasonable to think that small chemical compounds with micromolar-submicromolar potency in blocking selectively the AQP9 channel, may be effective in counteracting the aberrant hepatic fat accumulation underlying NAFDL/NASH, pathologies for which several potential therapeutic approaches have been proposed while no established therapy does exist (for a review see Calamita and Portincasa, 2007). The gene discussed is AQP9; the disease is metabolic dysfunction-associated steatohepatitis.