CALCA and pancreatic ductal adenocarcinoma: Similarly, the previous study of our research group also found that the CpG island methylation of CALCA and CALCB in pancreatic ductal adenocarcinoma was significantly higher than that in adjacent tissues and CGRP participated in cell proliferation, apoptosis, differentiation, and survival through the AKT/CREB signaling pathway and finally promoted the occurrence and development of tumors [33].