SOD2 inhibition in conjunction with NB increased ROS levels and inhibited PI3K/Akt signaling, while the inhibition of ROS increased PDAC cell proliferation even in the presence of NB, indicating a possibility for feedback regulation between ROS and PI3K/Akt signaling in NB-treated pancreatic cancer cells. The gene discussed is AKT1; the disease is familial pancreatic carcinoma.