To test whether fortilin changes its intracellular localization upon ER stress, we stimulated the PC3 human prostate cancer cell line with either thapsigargin (TG) or the epidermal growth factor (EGF) fused to the proteolytic A subunit of a bacterial AB5 toxin (SubA) (EGF-SubA), subjected cells to subcellular fractionation, and quantified fortilin concentrations in the nuclear, cytosolic, and ER fractions using immunoblot analysis. The gene discussed is EGF; the disease is Familial prostate cancer.