Specifically, we will discuss pharmacological strategies aimed to counteract the effects of pro-inflammatory stimuli (i.e., TNF-α, IL-6) in cachexia, sarcopenia and RA, as well vector-based micro-dystrophin transfer, oligonucleotide-induced exon-skipping and cell therapy strategy based on the use of healthy myogenic cell precursors [i.e., satellite cells, side population (SP), fibro-adipogenic progenitors (FAPs), mesoangioblasts, ES, and iPS cells] in dystrophinopathies (Figure 2). This evidence concerns the gene TNF and rheumatoid arthritis.