Although in PTEN null breast cancers, p110β activity was induced by G protein coupled receptor (GPCR) [14, 15], in our models of resistance to BYL719, p110β is activated in an IGF1R/IRS-dependent manner and contributes to AKT and mTOR activation, and ultimately to resistance to p110α inhibition. The gene discussed is AKT1; the disease is breast carcinoma.