The general effect of PIK3CA gain-of-function mutations in the sensitization to PI3K pathway inhibitors has been confirmed in a mouse model with inducible expression of human oncogenic p110α (i.e., p110α H1047R), where treatment of the p110α H1047R driven lung adenocarcinomas with the dual PI3K/mTOR inhibitor BEZ235 led to marked tumor regression (Engelman et al., 2008). Here, PIK3CB is linked to lung adenocarcinoma.