Beyond the obvious variations due to cancer-types, organ-of-origin for different tumors and disparate therapeutic or non-therapeutic contexts from which such analyses were derived, also non-necroptotic functions of MLKL or RIPK1/3 (e.g., RIPK1 as a scaffold/survival or RIPK1/3 as pro-apoptotic factors) could contribute to such inconsistencies. The gene discussed is MLKL; the disease is cancer.