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Necroptosis is a form of regulated necrosis that results in cell death and content release after plasma membrane permeabilization. However, little is known about the molecular events that mediate the disruption of the plasma membrane. Here, we have quantified the kinetics of calcium and propidium iodide influx during necroptosis using live cell imaging in multiple cell lines used as standard models in necroptosis research. In addition to the commonly used treatment to induce necroptosis via the TNF receptor, we examined other pathophysiologically relevant pathways, such as those involving Toll-like receptors (TLR) 3/4, with relevance during bacterial and viral invasion. We found that early calcium influx upon TNF-induced necroptosis in the presence of a Smac mimetic is mediated by ion channels and is cell-type dependent. Importantly, this early event is mediated by Smac treatment, does not require the activation of the necrosome machinery and is dispensable for necroptosis. Indeed, necroptosis induced by the activation of TLR3/4 pathways does not trigger early calcium influx. Moreover, using osmoprotectants of different sizes, we show that it is membrane pores of less than 4nm in diameter that mediate necroptosis execution in a cell- and treatment-independent manner. Strikingly, extracellular calcium is not required for pore formation. To our best knowledge, this represents the first evidence obtained in living cells regarding the role of membrane pores in necroptosis. Those pores allow the passage of small molecules and ions. Therefore, we settle the debate about ion influx in necroptosis signaling. In fact, our findings reconcile apparent contradictions about the essential role of different ions (i.e calcium or sodium) in necroptosis taking into account that different ions could pass through punched membranes. Collectively, our data demonstrate that early calcium influx does not modulate the size of the later pores formed in the plasma membrane.