For HCMV, mitochondrial MCSs begin increasing early (8 hpi) and continue throughout infection, especially for those involved in ER-tethering (e.g., VAP-A/B, MFN1/2), fission (e.g., DNM1L/2, MFF, TBC1D15), mitochondrial membrane integrity (e.g., SAMM50, MTX1/2, MIC60), and ER-mediated calcium transfer (e.g., PTPIP51, VDACs, HSPA9, ITPR3) (Fig. 1C). This evidence concerns the gene ITPR3 and infection.