It has been reported that inflammation plays a role in calcinosis cutis.[2] In juvenile dermatomyositis, the levels of serum interleukin-1, interleukin-6, interleukin-1B and tumor necrosis factor-A in patients with calcinosis are increased, and the denatured protein-bound phosphate of necrotic cells at the inflammatory site is increased, resulting in the formation of calcium deposition nests.[3] There is also evidence that vascular ischemia impacts the development of calcinosis cutis. Here, IL6 is linked to juvenile dermatomyositis.