Dysregulated PTMs—including phosphorylation, acetylation, ubiquitination, and glycosylation—alter key signaling pathways (e.g., NF-κB, STAT3, Wnt/β-catenin), metabolic reprogramming, and interactions with the tumor microenvironment, enabling MM cells to evade therapies such as PIs and IMiDs. This evidence concerns the gene NFKB1 and Miyoshi myopathy.