SLC7A11 and pancreatic ductal adenocarcinoma: In pancreatic ductal adenocarcinoma (PDAC) progression, PDAC-derived cancer-associated fibroblasts (CAFs), which mediate peritumoral fibrosis and the creation of the drug physical barrier, are highly dependent on SLC7A11 for cystine uptake and glutathione synthesis; related experiments showed that the nanogene-silencing drug treatment against SLC7A11 inhibited the growth and metastasis of PDAC, CAF activation, and fibrosis [26].