c-Maf has long been regarded as a therapeutic target of MM due to the following events: (1) c-Maf is highly expressed in MM promoted by chromosome translocation9, STAT3 and FGFR3 signaling transductions10,11, and others; (2) c-Maf transgenic mice develop myeloma-like syndrome23; (3) Genetic inhibition of c-Maf leads to MM cell death16,24; (4) c-Maf is mainly expressed in the early stage of embryonic development but not expressed in adult tissues except CD4 T cells25. Here, FGFR3 is linked to Miyoshi myopathy.