In agreement with these results, Chung et al., by transfecting mouse livers with different KRAS constructs, found that the survival of mice carrying mutation-activated KRAS-4A is significantly better than that of animals transfected with mutated KRAS-4B [16] and Luo et al. propose that the exon specifically included in KRAS-4A confers the gene a certain tumour-suppressor function [17]. The gene discussed is KRAS; the disease is neoplasm.