Moreover, studies using Rps6P-/- mice have shown that Rps6 phosphorylation facilitates Kras-dependent pancreatic cancer initiation [108] and Akt-driven pancreatic β-cell tumorigenesis [109], suggesting that Rps6 phosphorylation may also contribute to tumor development in ΔS6 livers, together with, or independent of the broader pro-oncogenic mTOR network. This evidence concerns the gene KRAS and neoplasm.