In our study, although the canonical TRAV1–2/TRAJ33 rearrangement was the predominant one featured in the TCR α-chain repertoire in HD and PRs, a clone of TRAV1–2/TRAJ34–expressing noncanonical MAIT cells dominated in one of the EC subjects, confirming that TRAV1–2 can use alternative TRAJ genes to generate MAIT TCR. This evidence concerns the gene TRAV1-2 and Huntington disease.