A broadly applicable model system for investigating how KRAS mutations modulate cellular phenotypes and MAPK signaling would ideally be characterized by (a) a tissue context or cell lineage in which Ras proteins regulate cell fate decisions and RAS mutations occur in cancer, (b) dependence on MAPK signaling for survival and proliferation, and (c) the flexibility to inducibly express individual mutant K-Ras proteins in the presence of endogenous levels of H-Ras and N-Ras. This evidence concerns the gene HRAS and cancer.