Because of the observed pathway enrichment of “human cytomegalovirus infection” in the RNA-Seq analysis of FGFR2 KO HaCaT cells (Figure 5B) and the previously demonstrated suppression of the expression of a battery of antiviral and/or pro-inflammatory ISGs in keratinocytes by FGF7 and FGF10,18 we determined if long-term genetic loss of FGFR2 in human keratinocytes has the opposite effect. Here, FGF10 is linked to cytomegalovirus infection.