It is therefore possible that in individuals predisposed to autoimmunity, such as those expressing the CD226 G allele, SARS-CoV-2 may tilt the immune balance toward CD155–CD226 interaction, generating “cytokine storms.” On the other hand, in persons with preexisting immune defects, such as immune senescence, the CD155–TIGIT interaction may be enabled, engendering more profound immune deficits (by adding immune exhaustion to the previously aged CTCs and NK cells) (107, 108). The gene discussed is PVR; the disease is Autoimmunity.