Indeed in a GEM model of breast cancer driven by Her2, knockout of p110α blocked tumor formation while knockout p110β actually caused tumors to develop more quickly- a surprising result explained by a competition model where the less active p110β binds to the same limiting number of p85/p110 binding sites on Her2 and thus actually lowers signaling output compared to the case where only p110α is expressed and hence can bind to all of the PI3K binding sites on the receptor (Utermark et al., 2012). The gene discussed is PIK3CA; the disease is neoplasm.