In any case, this scenario should be contextualized within the patho-physiological pattern and gender of the investigated animal and human specimens because the extent of AQP9 protein and liver import of glycerol had a distinct profile of control in n3-PUFA (ω3 polyunsaturated fatty acids)-depleted female rats [68], a model of metabolic syndrome having several features of the disease also including liver steatosis, and in rats [69] and mice [70] fed a high-fat diet. Here, AQP9 is linked to fatty liver disease.