Given previous in vitro studies demonstrating PLSCR1 induction by IAV (WSN) (Luo et al., 2018) and type 1 IFNs (Zhou et al., 2000; Dong et al., 2004; Lizak and Yarovinsky, 2012), we propose that the contradictory trend observed by Liu et al. may be attributed to distinct properties of SIV, such as viral replication rate, both the cellular tropism and the tissue tropism (proximal or distal lung), or antigen variation which may affect direct interaction with PLSCR1, innate sensing of the infection, or recognition by the adaptive immune response. This evidence concerns the gene PLSCR1 and infection.