One intriguing possibility is through the TRAF6-mediated K-63 ubiquitination and nuclear localization of hnRNPA1 during innate immune activation (Culver-Cochran and Starczynowski, 2018); if the activity of TRAF6 is inhibited during infection hnRNPA1 activity could drop, leaving TRA2-β pre-mRNA vulnerable to inclusion of the poison exon. This evidence concerns the gene TRA2B and infection.