The necessity of monitoring skeletal complications in LCH, which may result from direct disease-related bone infiltration and infarction, prolonged glucocorticoid therapy, or chemotherapeutic agents.[29] Cytokines like IL-1, IL-6, and TNF-α drive osteoclastogenesis and bone resorption in LCH through inflammatory pathways.[30] In this case, this patient experienced a femoral infarction prior to steroid initiation supports a primary contribution from LCH-associated bone disease, although subsequent lesions could be compounded by treatment effects. The gene discussed is TNF; the disease is Langerhans cell histiocytosis.