Constitutive BCL-2 expression could then contribute to the residual viability of glaucarubin-treated MCPyV-positive MCC cells that we observed in Figure 1B and Figure 6A. Previous efforts and our observations suggest that a combination of DNA damage and BCL-2 inhibition could effectively kill BCL-2-high, MCPyV-positive MCCs with low mutational burdens (Figure 6B). The gene discussed is BCL2; the disease is Merkel cell skin cancer.