A previous study reported that one of these factors is responsible for CXCL12 induction, and there is growing interest in FAPα protein as a potential target for CXCL12-expressing tumors because FAPα in carcinoma-associated fibroblast (CAF) directly controls CXCL12 levels in tumors, and the depletion of CAF-expressing FAPα from tumors permitted immune control of tumor growth in human pancreatic ductal adenocarcinoma 11. Here, FAP is linked to neoplasm.