Given that MSH3 is involved in double-strand break repair via homologous recombination, is able to facilitate nuclear-cytosolic shuttling of proteins, but can also induce DNA repair deficiency when over-/underexpressed, it is reasonable to envision an experimental context wherein MSH3 was tested to a) better elucidate the role of CoV nuclear import and its role in cancer, b) test drugs that prevent the import of viral proteins, and c) specifically target MSH3 for clinical applications. Here, MSH3 is linked to cancer.