To study the role of A2AR-CB1R heteromers in HD in vivo we analyzed their expression and function in a widely accepted model of HD, heterozygous mutant knock-in HdhQ7/Q111 mice, that express in heterozygosity a mutant full-length huntingtin allele with 111 glutamine residues, and wild-type HdhQ7/Q7 mice, that express two wild-type full-length huntingtin alleles with 7 glutamine residues. This evidence concerns the gene HTT and Huntington disease.