To identify conserved mechanisms driving these phenotypes we leveraged RIGI development in two cell lines to exclude tissue specific mechanisms, we selected am immortalized nearly normal bronchial epithelial cell line HBEC3-KT and the osteosarcoma epithelial cell line U2OS, which has been widely used to study mechanism of DNA damage and repair because of DNA repair pathways and cell cycle regulation preservation [41, 42]. This evidence concerns the gene RIGI and osteosarcoma.