Although CCL5 was not regulated in our system of persistent TNFα + IL-1β stimulation of TNBC cells, it is highly possible that chemokines such as CCL2, CXCL8 and CXCL1—which were increased due to the continuous cytokine stimulation and are known as having multiple promalignancy activities that are exerted on the cancer cells [43,63]—may upregulate tumor-promoting activities in the tumor cells themselves. The gene discussed is CCL5; the disease is cancer.