Tim-3 overexpression in breast cancer cells promotes cell proliferation, migration, invasion, and tumor-associated tubal formation and enhances chemoresistance to paclitaxel by activating the NF-κB/STAT3 pathway and its downstream genes (cyclin D1, matrix metalloproteinase-1, vascular endothelial growth factor, and E-cadherin). Here, HAVCR2 is linked to breast carcinoma.