Although the central role of sialylated glycan bindings between SARS-CoV-2 SP and RBCs in the severe morbidities of COVID-19 has been the focus of this paper, such SP bindings to the heavily sialylated platelets and endothelial cells (which have no ACE2 and minimal ACE2, respectively) also contribute significantly to these morbidities, as noted above. The gene discussed is ACE2; the disease is COVID-19.