As shown in Figure 4E, the knockdown of annexin A1 in CD8+ T cells from the PBMCs of HD partially mitigated the phosphorylation of PI3K-AKT and p65 signaling pathways activated by IL-33, whereas silencing of PI3K, AKT, and p65 did not affect annexin A1 expression, suggesting that PI3K-AKT and p65 pathways are downstream of annexin A1 in CD8+ T cells. This evidence concerns the gene CD8A and Huntington disease.