SOAT1 and viral infectious disease: Upregulation of these genes could be a secondary effect resulting from the dysregulation of pathway components, such as domeless and Socs36E, in G9a mutants, rather than from direct epigenetic regulation by G9a. Taken together, these observations suggest that G9a epigenetically regulates a subset of Jak-Stat genes in the adult fat body to shape their transcriptional response to virus infection.