Kawasaki Disease (KD) follows an excess innate immune response to viral pathogens. Several investigators have proposed involvement of the stimulator of interferon genes (STING) pathway inhibited upstream by aspirin and intravenous immunoglobulins [76]. The same mechanism may operate in COVID-19 where SARS–COV-2 binding to ACE2 increases STING pathway activation. In most instances, activation occurs during the second phase of illness with immune hyper-responses, decreased lymphocyte counts, increased monocyte populations that secrete cytotoxic cytokines and heightened B and T cell responses as well [77].