Additionally, our series of cell experiments demonstrated that ADGRG6 knockdown significantly inhibited while ADGRG6 overexpression enhanced the growth and metastasis of PAAD cells by regulating the expression level of mutated p53 (mutp53) protein, which exerted various gain-of-function (GOF) activities through EGFR and NF-κB signaling pathways. The gene discussed is TP53; the disease is pancreatic adenocarcinoma.