By blocking PI3K/Akt signaling and suppressing NF-κB activation via inhibition of the nuclear translocation and phosphorylation (serine 536) of nuclear NF-κB p65, ADI displays a highly significant synergism in anticancer activities against pancreatic cancer cells deficient in ASS expression in combination with GEM (Figure 8C). Here, AKT1 is linked to familial pancreatic carcinoma.