Conversely, transgenic mice overexpressing BAI1 exhibited reduced inflammatory markers, decreased AC presence, and disease remission, emphasizing the crucial role of BAI1‐mediated efferocytosis in maintaining homeostasis.[120] Given the significance of neovascularization in tumor progression, research demonstrates that heightened BAI1 expression, coinciding with increased TSR levels, can hinder angiogenesis, paradoxically fostering efficient efferocytosis. This evidence concerns the gene ADGRB1 and neoplasm.