In any event, the CaM antagonist CBP501, a modified-peptide, inhibited human NSCLC cell migration, EGF-induced invasiveness, and EMT by blocking the interaction between CaM with K-Ras, as well as metastasis formation by Lewis lung carcinoma cells, leading to inhibition of cytokine production by the tumor-associated macrophages [71,72]. This evidence concerns the gene EGF and neoplasm.