Consistent with these clinical outcomes, the validation cohort had a biomarker profile consistent with kidney disease, including higher serum creatinine and cystatin C. It also featured differences in endothelial dysfunction evident by higher angiopoietin 2 and fms-like tyrosine kinase, a proinflammatory immunosuppressed state manifested as higher tumor necrosis factor-alpha, interferon-gamma, soluble programmed death-ligand 1. The gene discussed is CST3; the disease is kidney disorder.