In RHD, development of valvular lesions appear to result from antibody deposition with upregulation of vascular cell adhesion molecule 1 (VCAM-1) at the surface of the valve followed by infiltration of primarily CD4+ and some CD8+ T lymphocytes that promote inflammation, fibrosis, and scarring of the valves disrupting cardiac function (21–28). Here, CD8A is linked to rheumatic heart disease.