Since sFlt1 is capable of sequestering and thus determining the circulating levels of VEGFA, and thereby preventing its signal transduction [29–31], and considering that plasma sFlt1 levels are elevated in different liver diseases [32, 33], an attempt was made to discern whether the differences in VEGFA levels in non-steatotic and steatotic livers resulting from the exogenous administration of VEGFA may be explained, at least partially by potential differences in the circulating levels of sFlt1. Here, VEGFA is linked to liver disorder.