The N6-methyladenosine (m6A) modification, for example, has recently been shown to upregulate lncRNA H19, which sponges miR-184 to promote CARM1 expression, thereby driving drug resistance in multiple myeloma [67].These networks converge on apoptotic regulation, where miR-184 has been shown to promote apoptosis via upregulation of caspase-3, caspase-8, and caspase-9 when its expression is increased, while reduced miR-184 expression leads to EPHX1 activation and suppressed apoptosis [49, 53]. The gene discussed is CASP3; the disease is plasma cell myeloma.