Given IRF4’s centralrole in MM tumorigenesis38 andthe absence of POU motifs in the MM ATAC-seq data, we postulated that POU2AF1might act as a transcriptional coactivator of IRF4 by forming a master regulatorcomplex, similar to the relationship between POU2AF2/3 and POU2F3 in SCLC-Pcells. Here, IRF4 is linked to Miyoshi myopathy.