Studies in colon cancer [122,123] and melanoma [110] cells demonstrated that constitutive K-Ras signaling inhibits Rho activation and actin stress fiber formation in a MEK-dependent manner, although the mechanism is different; whereas, in colon cancer cells, MEK-regulated expression of Fra-1 reduced actin stress fiber formation by inactivating β1 integrins, and in melanoma cells, B-Raf regulates stress fiber formation and focal adhesion turnover by control of Rnd3, which inhibits the Rho/ROCK/LIM kinase/cofilin signaling pathway. The gene discussed is KRAS; the disease is colonic neoplasm.