Upon viral infection, type I interferons (IFNs), such as IFN-a/b, stimulate the transcription of antiviral interferon-stimulated genes (ISGs) by triggering phosphorylation, dimerization of signal transducer and activator of transcription 1 (STAT1) and STAT2, formation of interferon-stimulated gene factor 3 (ISGF3) complex with interferon regulatory factor 9 (IRF9), and nuclear translocation of ISGF3 complex (Stark GR et al. 2012). STAT1 contains a nonclassical nuclear localization signal (NLS) sequence which is exposed only upon phosphorylation‑induced homo‑ or heterodimerization of STAT1 (Nardozzi J et al. 2010; Fagerlund R et al. 2002; McBride KM et al. 2002). In the cytoplasm, the nonclassical NLS‑containing STAT1 dimers are initially recognized by an adaptor molecule, importin subunit α‑5 (also known as karyopherin subunit α‑1 or KPNA1) (McBride KM et al. 2002; Nardozzi J et al. 2010). KPNA1 then recruits importin β‑1 (karyopherin subunit β-1 or KPNB1) via the N‑terminal importin β binding (IBB) domain of KPNA1 to form the NLS‑cargo:KPNA1:KPNB1 ternary complex (Cingolani G et al. 1999).