IFNAR1 and infection: Instead, we found that the fitness advantage of IFNAR1-disrupted cells during SARS-COV-2 infection was mediated by an increase in cell proliferation between days 4 and 8 post-infection (Fig. 4A and C), a finding that was mirrored by the antiproliferative response of uninfected Calu-3 and iPSC-derived type 2 alveolar epithelial cells to exogenous β-IFN treatment (Fig. 6G and H).