Thus, while prior studies have described endothelial heterogeneity in the tumor milieu, our work uniquely (i) captures the trajectory‐dependent orchestration of TF‐driven angiogenic programs in MM tumor cells, (ii) provides experimental validation that CREB3L2 knockdown modulates both angiogenesis and EMT‐related targets (e.g., increased E-cadherin, reduced vimentin), and (iii) delivers a prognostic model rooted in both single‐cell regulatory logic and bulk transcriptomic data. This evidence concerns the gene CREB3L2 and Miyoshi myopathy.