Because CD19 is a well-known marker for different types of myeloma clones and has been used as an immunotherapy target in MM treatment [19,20], we selected TNFRSF1A as the new candidate that may serve as a key regulator in the network; this gene was consistently upregulated in all three carfilzomib-resistant LP-1 cell samples (Fig. 3B). This evidence concerns the gene CD19 and Miyoshi myopathy.