Using the complementary approach of HMGN1-OE, the study concluded that HMGN1 facilitates leukemic transformation to DS-ALL due to its ability to generate a positive feedback mechanism resulting in the upregulated transcription of CRLF2 and dysregulation of the downstream signaling pathways and highlighted the crucial role of HMGN1 in DS-specific ALL. The gene discussed is CRLF2; the disease is acute lymphoblastic leukemia.