Importantly, an enzymatically inactive UTX variant also suppressed the growth of UTX-null human RPMI8226 cells and this together with the insignificant change in H3K27me3 in UtxΔ/ΔBrafV600E plasma cells compared to control by ChIP-seq, suggests that the demethylase activity is dispensable for the tumor suppressor function of UTX in MM. Here, KDM6A is linked to Miyoshi myopathy.