SH2D3C and viral infectious disease: In 2020, Claverie et al. hypothesized that STAT1 is a potential target of the SARS-CoV-2 NSP3 Mac1 domain of de-mono-ADP-ribosylation, which could lead to increased phosphorylated levels of STAT1 and higher expression levels of ACE2 that can result in increased viral infection [47].