However, these effects remain highly reversible prior to compensatory histone methylation switching, and deacetylation of H3K27 provides nucleation sites for reciprocal methylation switching, a feature that can be treated by concomitant repression of KDM6A/UTX and CREBBP/EP300 in MM [54] (Figure 4). Here, KDM6A is linked to Miyoshi myopathy.