For example, upon prolonged treatment of gemcitabine in pancreatic cancer, there is a rapid increase in histone acetylation at the promoters of pro-autophagy genes such as CSNK2A1 and analog metabolism genes such as Cytidine deaminase (CDA), resulting in both the degradation of gemcitabine in lysosomes as well as the conversion to inactive metabolites that are transported out of the cell [13,50]. Here, CSNK2A1 is linked to familial pancreatic carcinoma.