BCL2 and neoplasm: In a representative study, NK92MI cells were modified to load BCL‐2 targeting siRNAs into NK‐Exos, which upon uptake by ER+ breast cancer cells, led to potent downregulation of BCL‐2 expression.[282] This gene silencing effect triggered mitochondrial membrane disruption, caspase‐3/7 and caspase‐9 activation, and significantly enhanced apoptosis in tumor cells, while sparing nonmalignant counterparts.