Furthermore, ATXN1 has been shown to favor the toxicity of human pathogenic ATXN2 in mice-models; on the contrary loss of function of ATXN1 increased the stability of BACE1-mRNA, enhancing amyloidogenic cleavage of APP in a mouse model of AD (see Section 5.4.1) and outlining a function of ATXN1 also in AD (Suh et al., 2019). This evidence concerns the gene ATXN2 and Alzheimer disease.