We found that MILD COVID-19 patient exosomes had higher levels of the MHC class II receptor, which is responsible for antigen presentation to CD4+ T helper cells and high levels of both CD11b, a differentiation marker for cells of the myeloid–monocytic lineage (46, 47), and CD86, a type I transmembrane protein originally identified as a CD28/CTLA-4 ligand, which are both associated with T-cell activation (48). The gene discussed is CD86; the disease is COVID-19.