First, they used simvastatin to determine whether the inhibition of endogenous chol biosynthesis in prostate cancer cells could alter cell survival and signal transduction through the Akt serine-threonine kinase and its downstream effectors; simvastatin significantly decreased the chol content of lipid rafts, with consequent inhibition of Akt signaling and stimulation of apoptosis. The gene discussed is AKT1; the disease is prostate carcinoma.