IGF1R and Miyoshi myopathy: This regulation operates through the capacity of CD45 to facilitate either SRC kinase activity (IL6 signaling) when present at the surface of MM cells, or RTK activity (IGF1R/CD221 and IGF1 signaling) when absent since CD45 is a potent inhibitor of IGF1R (CD221) aberrantly expressed on MM cells (42, 43).