Additionally, etoposide treatment did not sensitize the MEF REV1 KO cells, suggesting that REV1 inhibition perhaps engages a different biological response that enables cancer resistance during strand breakages from IR or etoposide treatment, which contrasts with the reduction in mutagenesis and chemoresistance upon REV1 inhibition during cisplatin treatment or treatment with other drugs that make chemical modifications to DNA. Here, REV1 is linked to cancer.