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Persistent IFN\u2010\u03b3 signaling alters the bone marrow microenvironment by activating the JAK\u2013STAT1 pathway, which results in immunological imbalance, inflammatory amplification, and depletion of hematopoietic stem and progenitor cells (HSPCs). IFN\u2010\u03b3 disturbs HSPC quiescence and self\u2010renewal, interferes with thrombopoietin (TPO)\u2013c\u2010Mpl communication, and stimulates cytotoxic T\u2010cell\u2010dominant immunological responses. Simultaneously, IFN\u2010\u03b3 destabilizes local immunological homeostasis by disrupting immune crosstalk through the IDO1 axis and regulatory T\u2010cell (Treg) malfunction. 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