The GRN inference further uncovered outcome-specific regulatory modules, with <i>RUNX3</i>, <i>EOMES</i>, <i>ELK4</i>, and <i>REL</i> regulons enriched in TFR, whereas <i>FOSL2</i> and <i>MAF</i> regulons were enriched in relapse, and their downstream targets linked to IFN-γ signaling, metabolic reprogramming, and immunoregulatory feedback circuits.<h4>Conclusions</h4>This AI-enabled single-cell analysis demonstrates how NK cell state composition, differentiation trajectories, and regulatory network rewiring collectively shape TFR versus relapse following TKI discontinuation in CML. The gene discussed is RUNX3; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.