Virus infection is quickly followed by production of type I IFNs. These cytokines will antagonize viral replication but also act to inhibit T-cell expansion in a STAT1 dependent manner (top). Gil et al now show that rapidly dividing (CSFE¹⁰), virus-specific T cells overcome this block to proliferation by down-modulating the level of STAT1 protein available for transducing signals from the IFN-αβ receptor (bottom). Illustration by Kenneth Probst.