We focused on mutant KRAS4B (referred to as KRAS in the remainder of this paper), which is the KRAS splice variant that is prevalent in cancer and has been shown to require the C-terminal farnesyl group, the C-terminal poly-Lysine block and a membrane/lipid environment with negatively charged head-groups for biological function [3, 4, 32]. The gene discussed is KRAS; the disease is cancer.