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. Here, TFRC is linked to chronic myelogenous leukemia, BCR-ABL1 positive.