Because earlier studies have found in various non-prostatic cancer models that CR-1 can signal via phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT), and extracellular signal–regulated kinases 1/2 (ERK1/2) [9], we looked for perturbations of these kinases following transient overexpression of CR-1. The gene discussed is AKT1; the disease is prostate cancer.