Mucin1 enhanced the stability of HIF-1α and recruited HIF-1α and p300 to bind to the promoter of glycolytic genes such as enolase1 (ENO1) and phosphoglucomutase-2 (PGM2), upregulating their expression which contributed to increased glucose uptake and lactate production in pancreatic cancer cells [33]. This evidence concerns the gene HIF1A and familial pancreatic carcinoma.