Steroid-induced osteonecrosis of the femoral head (SONFH) is a non-traumatic osteonecrotic disorder characterized by persistent disruption of the bone marrow microenvironment, a process that cannot be fully explained by vascular insufficiency or bone tissue necrosis alone. Emerging evidence has identified marrow adipogenic lineage precursors (MALPs) as a bone marrow-specific mesenchymal cell subpopulation that plays a critical role in regulating marrow homeostasis, vascular remodeling, and bone turnover. However, the functional significance and pathological involvement of MALPs in SONFH remain insufficiently defined.This review integrated recent advances in MALP biology with the traditional Chinese medicine (TCM) theory of Wei deficiency-blood stasis-marrow atrophy, and systematically analyze the potential stage-dependent roles of MALPs in the initiation and progression of SONFH from the perspective of global bone marrow microenvironmental imbalance. Available evidence suggests that during Wei deficiency stage, long-term or high-dose glucocorticoid use may induce abnormal expansion of MALPs, accompanied by impaired marrow homeostatic regulation. During the blood stasis stage, MALPs participate in vascular regulation through the secretion of angiogenic factors, while their functional dysregulation disrupts microcirculatory reconstruction and markedly promotes osteoclastogenesis in a receptor activator of nuclear ractor kappa B ligand (RANKL)-dependent manner, thereby amplifying the coupling between vascular dysfunction and excessive bone resorption. In the marrow atrophy stage, MALPs undergo further fate shifts toward adipocytes and myofibroblasts, resulting in sustained loss of regulatory and reparative capacity, progressive exhaustion of marrow regenerative potential, and ultimately irreversible vascular compromise and structural bone damage.Collectively, MALPs should not be regarded merely as adipogenesis-related cells in SONFH, but rather as central regulatory nodes that dynamically participate in bone marrow microenvironmental remodeling across disease stages. Wei deficiency-blood stasis-marrow atrophy theory provides a coherent conceptual framework for understanding the stage-specific functional transitions of MALPs in SONFH. Further investigation into MALP plasticity and microenvironmental regulatory functions may offer novel mechanistic insights and support the optimization of TCM -based therapeutic strategies for SONFH.