In vivo pre-clinical studies have shown that combinations of PI3K and MEK inhibitors consistently result in improved tumour growth inhibition compared to either single agent, and in many cases cause regression in a variety of human tumour xenograft and mouse tumour models with a range of genetic backgrounds, including those with KRAS, BRAF and/or PIK3CA mutations, and/or PTEN deletions [6], [12], [17], [18], [19]. Here, KRAS is linked to neoplasm.