When cells within the gastric mucosa progress from metaplasia to dysplasia to cancer, they acquire a Fas Ag-apoptosis resistant phenotype. It is unusual to completely abolish the pathway, suggesting other forms of Fas Ag signaling may be important or even necessary for gastric cancer to progress. Little is known about alternate signaling of the Fas Ag pathway in gastric mucosal cells. Using a cell culture model of rat gastric mucosal cells, we show that gastric mucosal cells utilize a type II signaling pathway for apoptosis. Under conditions of low receptor stimulation or under conditions where apoptosis is blocked downstream of the death-inducing-signal-complex (DISC), Fas Ag signaling proceeds toward proliferative signaling. Under conditions favoring proliferative signaling, cFLIP is recruited to FLICE at the DISC complex and activates Erk1/2. Erk1/2 in turn activates NF-B. Erk1/2 stimulates proliferation, while NF-B activation results in upregulation of the anti-apoptotic protein survivin, further promoting proliferation over apoptosis. These results suggest that factors which inhibit apoptosis confer a growth advantage to the cells beyond the survival advantage of avoiding apoptosis, and in effect convert the Fas Ag signaling pathway from a tumor suppressor to a tumor promoter.