There was also no significant difference between patients and controls for the total numbers of either activating or inhibitory KIR (activating p = 0.47, inhibitory p = 0.45), nor any significant differences in any KIR gene frequencies between the high grade CIN samples derived from HPV 16/18 infection and those that were derived from non-16/18 infection (Table 2). This evidence concerns the gene KIR3DL1 and infection.