In agreement with the critical role of early IFN response in attenuating infectious state, another study finds that cells pre-treated with IFN-β or IFN-λ exhibit resistance to SARS-CoV-2 infection by significantly decreasing the virus copy number. Similarly, 3D culture organoids pre-treated with either IFN-β or IFN-λ led to reduced viral infection. Cells depleted for either IFNAR1 or IFNLR1 had an overall increase in the number of SARS-CoV-2 infected cells, suggesting the integral role of IFN signaling in attenuating viral propagation (Stanifer et al., 2020). Further, IFN response was adequate in younger patients compared to older ones, which may partly explain the higher risk of infection in older people (Wei et al., 2020). Additionally, people with comorbid conditions like diabetes – a condition associated with impaired IFN response, are more susceptible to SARS-CoV-2 infection, which further points toward the critical role of IFN signaling in the early clearance of the virus (Erener, 2020). However, a comprehensive and longitudinal analysis of the IFN response in mild/moderate patients is warranted to understand the functional consequence of this immune response throughout the disease and recovery. Overall, considering the relatively better IFN response and ISG expression induced by SARS-CoV-2, one can argue that this functional immune response is a probable reason for the relatively lower mortality rate seen in COVID-19, compared to previous SARS-CoV and MERS infections (Meo et al., 2020). However, these early findings warrant further proof.