These limitations highlight important directions for future research, including in vivo validation using appropriate animal models to confirm the role of BAIAP2L2 in PCa progression; more detailed mechanistic studies to elucidate the molecular pathways mediated by BAIAP2L2; investigation of potential interaction partners of BAIAP2L2 that might contribute to its regulatory role in PCa; and exploration of combinatorial approaches targeting multiple hub genes to maximize therapeutic impact. The gene discussed is BAIAP2L2; the disease is posterior cortical atrophy.