Pims are constitutively active following growth factor signaling in MM, with no mutated forms reported to date, though a high rate of somatic hypermutation involving the Pim genes is reported in other B lymphoproliferative malignancies.48, 49 The bone marrow microenvironment has a dominant role in upregulation of Pim-2 in MM. Here, PIM2 is linked to Miyoshi myopathy.