FAH and Tyrosinemia type 1: In another study, Balestra and colleagues [13] used a mouse model (FAH5961SB) for the Fumarylacetoacetate hydrolase (FAH) deficiency (also known as Tyrosinemia type 1) and demonstrated that a compensatory U1 snRNA expressed in AAV, and administered via the lateral tail vein was able to partially restore the normal splicing disrupted by a mutation at the last nucleotide of the mouse Fah gene exon 8 (c.706G>A).