Interferon-induced transmembrane proteins (IFITMs) are a family of host restriction factors that affect the fusion capacity of many enveloped RNA viruses. A preprint by Prelli Bozzo et al. now reports that SARS-CoV-2 appears to hijack IFITMs, and in particular IFITM2, as cofactors for the infection of lung cells. Whereas overexpression of IFITMs impaired SARS-CoV-2 membrane fusion with HEK293T cells in vitro, knockdown studies in the human lung epithelial cell line Calu-3 showed that endogenous levels of IFITM1, IFITM2 and IFITM3, both in the absence or presence of interferon, boost SARS-CoV-2 infection, with IFITM2 showing the strongest effect.