Using cell lines derived from mouse models of PDAC generated by knock-in p53 alleles carrying point mutations at codons R172H and R270H (equivalent to R175H and R273H in humans), we found that silencing p53R172H and p53R270H in pancreatic cancer cells significantly alters lipid metabolism, with patterns of common and variant specific changes. The gene discussed is TP53; the disease is pancreatic neoplasm.