Acute myeloid leukaemia (AML) is a life threatening hematologic malignancy. Despite a well-characterized genetic and molecular landscape, targeted therapies for AML have didn't considerably improve clinical outcomes. Over the past decade, proteasome inhibition has been incontestable to be a good therapeutic strategy in many medicine malignancies. Proteasome inhibitors, like bortezomib and carfilzomib, became mainstays of treatment for myeloma and mantle cell malignant neoplastic disease. In light-weight of this success, there has been a surge of literature exploring each the role of the proteasome and also the effects of proteasome inhibition in acute myeloid leukaemia. Pre-clinical studies have incontestable that proteasome inhibition disrupts proliferative cell sign pathways, exhibits cytotoxic synergism with different chemotherapeutics and induces autophagy of cancer-related proteins. Meanwhile, clinical trials incorporating bortezomib into combination therapy regimens have reported a variety of responses in AML patients, with complete remission rates. In a trial to focus additional investigation into this space, these recent studies and their findings are reviewed here.