In summary, our data demonstrate for the first time that stroma-, but not hypoxia-induced upregulation of JunB is a critical, MEK/MAPK- and NFκB-dependent but Ras-independent mediator for the transcription of key AFs VEGF, VEGFB and IGF1, and thereby MM BM angiogenesis, particularly in early MM (Fig. 7). Here, JUNB is linked to Miyoshi myopathy.