EGFR and carcinoma: In two transformed murine fibroblast cell lines, stable transfectants overexpressing the human EGFR, mimicking the overexpression of this receptor observed in many carcinomas, it was observed that a myristoylated myosin light-chain kinase (MLCK) peptide, which sequesters endogenous CaM or the CaM antagonists W-7 (N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide) and W-13 (N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide), inhibited the EGF-dependent activation of the receptor [44].