For example, whole body CgB knockout (KO) provided an insulin secretory defect that was unable to be explained aside from a small decrease in the number of docked SGs [162], whereas adenoviral knockdown (KD) of CgB in INS1-832/3 insulinoma cells and isolated mouse islets resulted in marked insulin secretory defects that could be explained by a defect to SG biogenesis [159]. This evidence concerns the gene INS and pancreatic insulinoma.