The inherent plasticity of AECII allows them to rapidly express GM-CSF in response to viral infection, or via induction by inflammatory cytokines, such as IL-1β, TNF-α, and in turn, expression of GM-CSF influences AECII plasticity in an autocrine fashion, inducing downstream STAT5 phosphorylation and subsequent upregulation of cyclin D1 and other cell cycle genes that regulate differentiation of AECII into AECI (Cakarova et al., 2009; Mir-Kasimov et al., 2012; Sturrock et al., 2012). This evidence concerns the gene CSF2 and viral infectious disease.