An abundance of inhibitory factors, such as TGF-β, may be partially responsible for the NK cell hyporesponsiveness observed in COVID-19 patients. In support of this hypothesis, Huang et al. found significantly higher TGF-β levels in SARS patients compared to healthy controls and this positively correlated with length of stay (138). Given the importance of TGF-β in suppressing NK cell functions, it is possible that the higher levels of TGF-β (as well as other inhibitory cytokines) in CoV patients leads to suppression of NK cell antiviral activity (138). Early studies of COVID-19 patients report secondary (super-) infections, including nosocomial pneumonia or bacteremia as a complication of SARS-CoV-2 infection (138). Since NK cells are critical first responders that play a role in preventing and clearing infections (139), a poor NK cell count or exhausted phenotype, in addition to negatively influencing COVID-19 patient outcomes, could facilitate the development of secondary infections and have a significant negative impact on patient outcomes.