For example, during HIV infection, it has been shown that viral proteins hijack E3 ligases and the ubiquitin proteasome system to target host factors to reduce superinfection (i.e., CD4 and CXCR4) (61), increase viral transcription (i.e., IκBα) (62), promote viral infectivity (i.e., SERINC5, PSGL-1, SMUG, and UNG2)(61, 63, –, 65), and inhibit innate immune response (APOBEC3G/F/H, Tetherin) (66, 67). This evidence concerns the gene CD4 and HIV infectious disease.