Similar to established tumours in GEMMs, there was no clear differences in ERK, AKT and S6 activation between human KRASG12C and KRASG12D cell lines (Fig. 4F), again likely due to factors such as genomic heterogeneity between cell lines or Epithelial-Mesenchymal Transition influencing pathway activation [38]. The gene discussed is AKT1; the disease is neoplasm.