In an effort to settle the controversial role of the XPG/RAD2 C-terminal region in the pathogenesis of CS, we attempted to investigate the unknown functions of yeast RAD2. We analyzed multiple rad2 C-terminal deletion (rad2CΔ) mutants to define the sequences responsible for the CS-like phenotypes and examine the roles of those sequences in various cellular mechanisms. This evidence concerns the gene FEN1 and Cowden syndrome 1.