Despite the seemingly insufficient inhibition of pERK, we observed a robust inhibition of anchorage-independent growth and tumor growth in vivo, suggesting that other farnesylated proteins (including Rheb, Rac1, RhoB, mTOR/Raptor, lamins A/B and CENP-E/CENP-F [62–64]) outside of the MEK/ERK pathway could be contributing to the growth inhibitory effects of tipifarnib. The gene discussed is MTOR; the disease is neoplasm.