The rationale for these studies is that TNFα is mitogenic to mesothelial cells [14], causes MM cell transformation [13], and may have pleiomorphic effects on inflammation and/or cell defense as it is linked to both upregulation of the mitochondrial antioxidant enzyme, manganese-containing superoxide dismutase (SOD2) [15], as well as increased chemokine production by lung macrophages and neutrophils after pathogenic particle exposures [16]. This evidence concerns the gene SOD2 and Miyoshi myopathy.