To further explore the potential role of the ADGRG6-mutated p53 signaling axis in pancreatic cancer, by constructing a CFPAC-1 cell model in which mutated p53 (C242R) was reintroduced following ADGRG6 knockdown, we observed that the inhibition of proliferation, migration, and invasion caused by ADGRG6 knockdown was substantially reversed by the overexpression of exogenous p53(C242R) (Figures 10A–C). This evidence concerns the gene TP53 and pancreatic neoplasm.