Conversely, when we overexpressed ADGRG6 in MIAPaca-2 cells with endogenous p53 (mutp53) knockdown beforehand, the regulatory effects of ADGRG6 overexpression on proliferation, migration, invasion and the expression of the proliferation-, EMT- and immune-related markers of PAAD cells were greatly impaired when endogenous p53 was knocked down, suggesting that ADGRG6 mediated these effects through mutated p53 in PAAD cells (Figures 10D–H). The gene discussed is TP53; the disease is pancreatic adenocarcinoma.