The results showed that ADI combined with LY294002 at 20 μM significantly down-regulated the level of p-Akt (Thr308) and p-p65 (Ser536), but not p-ERK1/2 (Thr202/Tyr204) in ASS-deficient PANC-1 cells, as compared to ADI treatment alone (P < 0.05) (Figure 7A); however, the combined treatment of ADI and LY294002 did not change the expression of relevant proteins of the PI3K/Akt and NF-κB p65 signaling pathways as compared with ADI treatment alone, in ASS-positive BxPC-3 pancreatic cancer cells (Figure 7B). The gene discussed is NFKB1; the disease is familial pancreatic carcinoma.