Considering the viability data of infected melanoma and glioblastoma (Figure 1) cells, together with control non-tumor cells (Figure 3), it was suggested that both cathepsins contribute to the reovirus infection of tumor cells, in contrast to cathepsin S. Furthermore, for the cells used in this study, the contribution of cathepsin L was more crucial, as cells remained permissive to reovirus-mediated oncolysis in the absence of cathepsin B activity. The gene discussed is CTSB; the disease is glioblastoma.