The expression of KIT is a hallmark of seminomatous TGCT, reflecting their early germ cell origin, and its levels can be modulated by exogenous activin A in both seminoma‐derived TCam‐2 cells, with an increase in transcript levels,52, 67 and in seminoma tumour fragment hanging drop cultures, with decreased transcript and protein levels.50 The gene discussed is KIT; the disease is neoplasm.