In addition, BTN3A2's potential to regulate immune responses through its interaction with other butyrophilins, such as BTN2A1, which is involved in pathogen recognition and immune activation, further supports the hypothesis that butyrophilins‐mediated Vγ9Vδ2 T cell activation can modulate stroke‐related immune mechanisms in a more precise way compared to traditional anti‐inflammatory therapies. This evidence concerns the gene BTN3A2 and stroke disorder.