Together, these data not only confirm expression of some of the markers associated to the TRM phenotype in other tissues25,26 in cervical CCR5+ TRM, but also strongly suggest two concepts related to our hypothesis: (1) TRM express several molecules that may render them highly susceptible to HIV infection (namely α4β7, CXCR4, CXCR6 and CCR6), and (2) these cells are potentially self-renewed and maintained long-term in tissues (i.e., CD122, CD132, CD127). This evidence concerns the gene CCR6 and HIV infectious disease.