Recent evidence further suggests that tumor-intrinsic regulators of autophagy can indirectly modulate TAM function: for example, inhibition of heparanase (HPSE) by the small molecule RDS 3337 in U87 glioblastoma cells was shown to block autophagic flux (LC3-II and p62/SQSTM1 accumulation) and trigger apoptosis (caspase-3 activation and PARP1 cleavage), highlighting how disrupting tumor-cell autophagy can rewire cell death pathways and potentially reshape the immune microenvironment [59]. Here, PARP1 is linked to neoplasm.