CRISPR/Cas (Clustered regularly interspaced short palindromic repeats/CRISPR-associated system) is originally a self-protecting mechanism in bacteria against external DNA such as virus genome or plasmids. Its major player: CAS9 endonuclease cuts the external DNA and induces mutation by NHEJ (Non-homologous end joining), making the external DNA loss its biological activities. HIV (Human immunodeficiency virus) is the trigger of the lethal disease AIDS (Acquired immune deficiency syndrome). It replicates in and kills the helper T cells, weakening the human immune system. Traditional therapies like chemotherapy or radiotherapy can’t protect the helper T cells from virus invasion and the virus can lurk in the helper T cells; drug treatment like reverse transcriptase inhibitors, protease inhibitors and entry or fusion inhibitors are not very effective due to the high mutation rate of HIV and their amount of usage is also limited due to the side-effects. In this project, we want to establish a more effective HIV-curing system with less side-effects by integrating CRISPR/Cas9 system into human hemopoietic stem cells, which aims to protect the helper T cells from virus infection. The sgRNA is designed to target the relative conserved regions in HIV virus DNA genome which encodes essential parts for HIV survival and replication like reverse transcriptase or integrase and have limited mutation potential. Using A-B-toxin-based DNA delivery system to deliver plasmids encoding sgRNA into the helper T cells, we can readily attack multiple HIV genome sites simultaneously and update the targets along with our knowledge of HIV.