Further, Yuan et al. highlighted the ability of P. gingivalis to evade immune surveillance, and they determined that the blockade of immune-checkpoint B7-H4 and lysine demethylase 5b in ESCC conferred resistance against P. gingivalis infection and tumor challenge, proposing them as potential therapeutic targets for controlling P. gingivalis infection and its associated neoplasia [86]. This evidence concerns the gene KDM5B and neoplasm.