To date, the roles of Fas and FasL in CC are not clear; cervical Fas levels have been reported not to change significantly, while FasL overexpression by tumor cells, ranging from 53 to 94%, has been considered as an evasion mechanism through which tumor cells kill cytotoxic T lymphocytes by apoptosis, which has been linked with carcinogenesis development (26-28). This evidence concerns the gene FASLG and neoplasm.