Through the comparison of the proteomic profile of intratumor cell populations in different degrees of differentiation, we demonstrated that the malignant phenotype may have arisen as a consequence of alterations in the expression of key proteins such as FNDC1, A1BG, CANX, HSPA5, and PDIA3 and that most of these variations may be involved in tumor evasion against inflammatory cells facilitating cancer spreading. The gene discussed is CANX; the disease is neoplasm.