found that tumor tissues from anti-TIF1γ-positive CAM patients showed increased genetic alterations such as somatic mutations and loss of heterozygosity (LOH) in TIF1 genes, and higher expression of TIF1γ compared to anti-TIF1γ-negative myositis patients, suggesting a role of TIF1γ in the pathophysiology of CAM (82). This evidence concerns the gene TRIM33 and neoplasm.