Interestingly, Ezponda et al. not only showed that loss of UTX/KDM6A leads to changes in the transcriptional profile of multiple myeloma (MM) cells contributing to the pathogenesis of the disease, they also revealed an increased in vitro and in vivo sensitivity of UTX/KDM6A-mutant cells to EZH2 inhibition, which rebalanced H3K27me3 levels of specific genes, revealing therapeutic strategy in MM cases harboring UTX loss-of-function mutations [82]. Here, KDM6A is linked to AL amyloidosis.