As our transcriptional profiling studies consistently found PHLDA2 as an immediate downstream target of EGFR/ErbB2 signaling, we speculated that PHLDA2 might have key inhibitory functions in EGFR and ErbB2-driven cancer cells and a better understanding of its functions might help define novel therapeutic options, in particular through yielding novel ways of interfering with phosphatidyl inositol-mediated activation of oncogenic AKT-driven pathways. The gene discussed is AKT1; the disease is cancer.