Necrotic cell death (necrosis) widely occurs in human pathologies, however, the therapeutic strategies to suppress it are still lacking due to our inadequate knowledge on its molecular mechanisms. One of the morphological markers of necrosis is nuclear condensation (pyknosis), which has been used widely to distinct from apoptosis. However, the molecular mechanism of necrotic pyknosis and its functional role in necrosis propagation are still unclear. To address these questions, we generated a genetic model in Drosophila to temporally follow the progression of necrotic pyknosis. Surprisingly, we observed an intermediate state of chromatin detachment from the nuclear envelope (NE), followed with the NE completely collapsed onto chromatin. This phenomenon leads us to discover that phosphorylation of barrier-to-autointegration factor (BAF) mediates this initial separation of NE from chromatin. Functionally, inhibition of BAF phosphorylation suppressed the necrosis in both Drosophila and human cells. This suggests that necrotic pyknosis is an essential and evolutionally conserved step for the propagation of necrosis. Therefore, BAF phosphorylation may represent a biochemical marker of necrosis and potentially serve as a therapeutic target for necrosis-related diseases.