Moreover, in breast cancer cell, the accumulation of U-STAT3 in response to ER stress induces endogenous expression of CCL5 and inhibition of CCL5 secretion leds to decrease in transmigration of breast cancer cells.[53] IL-6-induced U-STAT3 accumulation also leads to an increase in CCL5 expression.[30,31] It is worth emphasizing that the accumulation of U-STAT3 seems contribute to inhibit the transmigration of breast cancer cells which reminds researchers the beneficial side of the U-STAT3 should be taken into account. The gene discussed is CCL5; the disease is breast cancer.