The GVL effect is based on the capability of immune cells to engage with tumor-specific antigens, minor histocompatibility antigens, and mismatched human leukocyte antigens (HLAs) on the leukemic cells.2 Although the interaction between 2 immune systems with incompatible HLAs poses the risk of graft-vs-host disease (GVHD), incompatible HLAs are also a dispensable source of the GVL effect in haploidentical HSCT.3 However, relapse has continued to surpass toxic effects on organs, infectious events, and GVHD, becoming the predominant cause of death after HSCT.4 The gene discussed is HLA-S; the disease is neoplasm.