Fig. 7.

Potential inhibitory interactions between the mTOR and NFkB pathways activated by Everolimus. It is suggestive that Everolimus disables IKK by p-mTOR, thus restraining the phosphorylation of IKb. This event prevents the migration of p65, as NFkB component, to the nucleus where it normally acts as transcription factor for M-CSF, TNF-α, IL-6, IL-1β and MIP-1α. This ultimately leads to an inhibited secretion of the pro-OC soluble mediators coded by these genes