S100A1 and neoplasm: To rule out the possibility that tumor-intrinsic S100A1 might contribute to the implantation of tumors, we used a doxycycline (Dox)-inducible system to abrogate S100A1 expression in LLC model (Supplementary Fig. 4c, d) and found that Dox-induced S100a1 loss attenuated the growth of established tumors and extended the survival of tumor-bearing mice (Supplementary Fig. 4e), similar to the results of the tumors transfected with the constitutive S100a1 shRNA.