Together, the processing of multiple epitope forms and intraepitope mutations resulted in a relative decrease in the binding strength between KIR3DL1 and the HLA-B∗27:05-peptide complex, which likely decreases inhibitory KIR signaling and the NK response to HIV-1 infection (Boudreau et al., 2016; Saunders et al., 2016). This evidence concerns the gene KIR3DL1 and HIV-1 infection.