Further investigations indicated the indispensable role of JunB in MM, including promoting cell survival, proliferation and drug resistance, as well as activating the transcription of pro-angiogenic factors (AFs), such as VEGF, VEGFB, and IGF1, and eventually leading to angiogenesis of bone marrow in MM models (Fan et al., 2017; Fan et al., 2021). This evidence concerns the gene JUNB and Miyoshi myopathy.