Given its role in innate immunity, PP4 has been initially reported as an activator of NF-κB-dependent transcriptional responses through its dephosphorylation of the c-Rel subunit of the NF-κB transcription factor.227 In viral infection conditions, direct binding of PP4 to TANK binding kinase 1 (TBK1) was reported to cause dephosphorylation of TBK1 at Ser172 and inhibition of TBK1 activation. Here, PPP4C is linked to viral infectious disease.