In fact, mutations affecting the activity of PRC2 complex are present in 40% of ETP-ALL patients and highly associated with activating mutations of the IL7R/JAK/STAT pathway [35] which gives relevance to using human LOUCY ETP-ALL cell line to model to study the biology of ETP-ALL leukemia [4, 36]. The gene discussed is SOAT1; the disease is leukemia.