The molecular mechanism that might explain the discrepancy between infection and activation of HGEC for the expression of SOCS-3 remains to be elucidated, but this discrepancy certainly reflected the activation of a different signaling pathway in host immune/inflammatory responses to LPS-Pg, as demonstrated in human monocytes infected with live P. gingivalis and stimulated by its purified LPS or its major fimbrial protein, fimbrillin (FimA) [30]. This evidence concerns the gene SOCS3 and infection.