The idea that RBPMS could be involved in the drug resistance of cancer cells originated in the studies of Rastgoo et al., who showed that increased levels of the enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb complex (PRC2), contributes to drug resistance in multiple myeloma (MM) by downregulating RBPMS [56]. This evidence concerns the gene EZH2 and AL amyloidosis.