The fact that we observed increased T-cell activation in this model, which is resistant to the antitumor effects of eribulin due to P-glycoprotein expression [55] such that tumors grew at the same rate regardless of drug treatment, demonstrates that the eribulin-mediated activation of CD4+ T-cells is dependent on the presence of a tumor, but independent of direct cytotoxicity against the tumor. Here, CD4 is linked to neoplasm.