While altered splicing of the K-ras proto-oncogene in favour of K-ras 4B could, conceivably, modulate tumour progression, and possibly by effects on MMP-2 expression, apoptosis and/or differentiation (see Background), the present study found that alteration in the ratio of the K-Ras proto-oncoproteins in favour of K-Ras 4B (by targeted deletion of K-ras exon 4A) does not affect mouse survival or tumour number, size or histopathology (including mitotic and apoptotic counts). The gene discussed is KRAS; the disease is neoplasm.