AKT1 and cancer: In OSCC, P. gingivalis has been shown to aid in the progression of cancer by (i) activating the expression of NF-kappaB and MAPK pathways, (ii) inhibiting apoptosis by activating jAk/stat and P13K/Akt, (iii) promoting angiogenesis by increasing expression of EENB2, (iv) increasing cell proliferation via PDCD4 inhibition, increasing AP1 and CD1, and (v) evading the host immune system through the production of butyric acid causing T-cell and B-cell apoptosis to ensure its survival on gingival epithelial cells [34].