Mechanistically, although both RNA Pol I inhibitors effectively suppress rRNA synthesis and activate the Nucleolar Stress Response (NSR), their distinct ability to induce DNA damage [15–18] impacts on HLA-E expression levels in MM cells, a ligand for the cognate receptor heterodimer CD94/NKG2A which inhibits NK cell function [19–21], and the CD94/NKG2C, an activating receptor [22, 23]. This evidence concerns the gene KLRC1 and Miyoshi myopathy.