MLKL and neoplasm: And given that MLKL-overexpression and MLKL-knockout did not exhibit opposite effects on primary tumour size in vivo, it reflects the necroptosis-independent role of MLKL; We did not completely abolish the necroptosis-independent role and necroptosis-dependent role of MLKL through MLKL knockout, but we introduced exogenous MLKL into RIPK3null PANC1 and RIPK3high AsPC-1 cells to simulate MLKL-driven necroptosis, which both leads to the consist subsequent TME events that promote tumour metastasis7,57–59.