While studying the formation of cytoplasmic RIG-I-containing stress granules upon infection of cells with Sendai virus or stimulation with the RIG-I ligand poly(I:C), Joo-Yeon Yoo and colleagues found that the joint stimulation of infected cells with TNFα and IFN-γ interfered with RIG-I granule formation and that FAT10 was the cytokine-induced factor that caused this effect [39]. This evidence concerns the gene IFNG and infection.