Mechanistic studies demonstrated thatthe concurrent restoration of PTEN and inhibition of AR induce significantapoptosis through caspase-3 activation, decrease cell proliferationby inhibiting the PI3K-AKT and extracellular signal-regulated kinase(ERK) signaling pathways, and disrupt AR-mediated pro-growth signaling.We expect that this approach of LNP delivery of siRNA and mRNA couldbe robustly expanded to many other tumor suppressors and tumorigenicdrivers for a fundamental biological understanding and therapeuticdevelopment. This evidence concerns the gene PTEN and neoplasm.