Computational analysis to identify miR-144 binding sites in the coding and non-coding sequences of the genes that belonged to this expanded network suggested only three candidates where we could hypothesize plausible mechanisms connecting them to our observed viral infection phenotype: Tpl2/Map3k8, Trim30, and Traf6, which each have at least one predicted canonical target sequences in their 3’-UTRs. Here, TRAF6 is linked to viral infectious disease.