The relevance of this in SARS-CoV-2 infection is highlighted by the impact of indoxyl sulfate on the endothelial dysfunction and CVDs associated with fatality in end-stage renal disease, and which is mediated via alterations in T cell function [162], with its detrimental effects, like other AhR agonists, driven by RhoA/ROCK path upregulation in endothelial cells [163]. This evidence concerns the gene RHOA and endothelial dysfunction.