Although the postmortem samples available for our study does not allow one to conclude on TREM2 cortical expression levels in HD nor to assess whether such a reduction of microgliosis around mutant huntingtin protein inclusions exists in the cortex of TREM2 R47H HD patient carriers, it will be interesting to look at whether this could underlie the link between the more aggressive cognitive decline suggested by our genotype–phenotype study in TREM2 R47H HD patients. The gene discussed is TREM2; the disease is Huntington disease.