In this report, we have shown that K17 overexpression in MmuPV1-induced papillomas supports persistent papilloma growth by suppressing the CXCL9/CXCL10/CXCR3 signaling axis and downregulating T cell recruitment to papillomas, indicating a novel role of K17 in contributing to MmuPV1 infection by affecting CXCR3 axis. The gene discussed is CXCR3; the disease is infection.