Several mitigating factors, including redundancy with farnesylation-independent orthologs or collateral signaling pathways, varying sensitivity to FTase activity between substrates [70], and pharmacokinetic compartmentalization, may render FTIs more selective in vivo, but mounting evidence supports the notion that farnesylated target oncoproteins including HRAS, RHEB, and RHOB could be exploited as part of FTI-anchored combination regimens in SCCs and a range of other tumor types. Here, RHEB is linked to neoplasm.