Briefly, in NSCLC we found [14]: 1) upregulation of both SULFs at the transcript level; 2) SULF2 protein expression in 20 of 20 human NSCLC tumors with minimal levels in normal lung; 3) SULF2 protein promotes the in vitro malignant phenotype, and the tumorigenicity in mice of SULF-2 positive human NSCLC cell lines; and 4) SULF2 promotes human lung carcinogenesis by regulation of Wnt signaling and the kinase activity of three critical receptors (i.e., EGFR, IGF-1R and cMet) (unpublished). The gene discussed is IGF1R; the disease is non-small cell lung carcinoma.