KLRB1 and Huntington disease: While the functional capacities of Tregs were not studied in this manuscript, based on this previous published work, expanding Tregs using Rapamycin could be promising, particularly if it could be confirmed that the expansion process is reducing the number of cells producing IL-17, as demonstrated by Afzali et al. More interestingly, an unbiased analysis using CITRUS (Figure 7) confirmed that HS patients had more of a CD161+ effector Tregs from population III (CD4+CD25hiCD127loCD45RA−) (cluster iii) compared to unsensitised HD.