KRAS and neoplasm: In addition to the RAF and PI3K cascades, RAS-GTP engages several additional effectors with RBDs,49 including RALA/B,73 which are implicated in the regulation of endocytosis, actin organization, proliferation and proinflammatory signaling through NFκB and RASSF1A, a tumor suppressor that stimulates proapoptotic signaling.50 It is plausible that different mutations of KRAS stabilize distinct conformational states that potentially differ in their affinity for the RBD of interacting effectors and thus alter the organization of the signaling network.74