Farnesyltransferase inhibitors (FTIs) were designed to block the action of Ras oncoproteins which depend on posttranslational modification by adding a farnesyl isoprenoid membrane anchor.  However, off-target actions are believed to account for most of their antitumor activity.  We recently reported the induction of autophagy in cancer cells in a dose-dependent manner by FTIs.  We observed similar results of autophagy in a panel of tumor cell lines for the three FTIs tested.  Therefore, the induction of autophagy is very likely a pharmacological class effect of inhibition of farnesyltransferase.  In this addendum, we discuss the possible mechanisms underlying the induction of autophagy by FTIs, including reactive oxygen species-, DNA damage- and Ras-mediated pathways as alternatives to Rheb-mediated regulation of mTOR and autophagy.