However, the viability of HMEG cells treated with PGE2 in combination with Regorafenib was significantly higher than with Regorafenib monotherapy (Fig. 6d) supporting the hypothesis that Regorafenib-induced COX2-PGE2 signaling seems to be a second independent mechanism facilitating tumor resistance and progression independently of the tumor cell-autonomous Bcl-2 upregulation. The gene discussed is PTGS2; the disease is neoplasm.