These results extend our understanding of MM biology by delineating the dynamic interplay between transcription factor–driven regulatory networks (particularly CREB3L2) and angiogenic programs at single‐cell resolution, highlighting the prognostic utility of combining single‐cell regulatory features with bulk gene‐expression signatures, and revealing potential therapeutic targets—for example, CREB3L2‐mediated pathways—that may be exploited to inhibit aberrant angiogenesis and overcome treatment resistance. This evidence concerns the gene CREB3L2 and Miyoshi myopathy.