Viral infection or serine metabolism defects increase expression of ATP6V0d2 by inhibiting S-adenosylmethionine-dependent H3K27me3 occupancy at the promoter, alleviating YAP-mediated blockade of the TBK1-IRF3 axis and thereby increasing IFN-β production (Shen et al., 2021). Here, IRF3 is linked to viral infectious disease.