In our study of AT/RT patient-derived tumor cell lines and patient tumor tissue, we found that the expression of human endogenous retrovirus K (HERV-K, sub-type HML-2) was facilitated by the LOF of SMARCB1 and that the expression of HML-2 proteins was critical for tumorigenesis and the maintenance of pluripotency [10]. The gene discussed is CLEC10A; the disease is neoplasm.