HMGCR and acute myeloid leukemia: Recently, Hong and colleagues described that AML-derived sEVs promote chemoresistance by an autocrine mechanism: AML blasts become chemoresistant due to the presence of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HMGCR) on AML-derived sEVs, which upregulates cholesterol synthesis followed by a massive release of HMGCR+ sEVs into the extracellular space, perpetuating this vicious cycle that acts against the efficacy of chemotherapy (63).