This is because (i) mRNA and protein levels of RIPK3 were upregulated after cisplatin treatment; (ii) knockdown of RIPK3 by shRNA prominently attenuated cisplatin-induced necrosis in the SMAC-deficient KYSE140 cells; (iii) the necrotic complex including RIPK1, RIPK3 and MLKL was formed, and the expression levels of its components increased; (iv) overexpression of exogenous RIPK3 still maintained the sensitivity of KYSE410 cells to cisplatin in the presence of caspase inhibitors; (v) RIPK3 overexpression reduced xenograft tumor growth. The gene discussed is MLKL; the disease is neoplasm.