Interestingly, this seems to resemble the mechanism by which the mouse model of Tay-Sachs disease (β-hexosaminidase A deficiency, GM2 gangliosidosis) is able to escape the human disease (via degradation of GM2 to GA2 via murine neuraminidases) in contrast to the human population where neuraminidase levels are lower [83]. This evidence concerns the gene ETFA and Tay-Sachs disease.