In addition, treatment with GY1-22 significantly reduced mutp53 expression, enhanced Waf1p21 expression, suppressed cyclin D1 expression, and inhibited mutp53-driven pancreatic cancer growth both in vitro and in vivo, indicating that DNAJA1 is critical for chaperoning mutp53’s stability and oncogenic function and is a potential robust therapeutic target for developing the efficient small molecule inhibitors against oncogenic mutp53. Here, CCND1 is linked to familial pancreatic carcinoma.