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Brenner's position is that it's a liability: charged molecules don't cross membranes, so NMN must shed its phosphate and enter cells as NR anyway — making NMN, in his words, a molecule that "doesn't get into cells as NMN."[13] The NMN camp counters with the 2019 discovery, from Shin-Ichiro Imai's Washington University lab, of Slc12a8 — a dedicated NMN transporter that would let NMN enter certain tissues intact.[11] This is a live, unresolved dispute, not settled fact: the transporter finding drew a pointed same-journal rebuttal titled "Absence of evidence that Slc12a8 encodes a nicotinamide mononucleotide transporter," and the groups have exchanged formal replies.[12] (The commercial stakes are real too — the transporter patent was licensed to Japanese corporation Teijin.[14]) Step back, though, and the feud mostly dissolves, because both molecules demonstrably raise intracellular NAD+ in humans, and the physicians least prone to hype treat them as effectively interchangeable.[22] For anyone deciding what to take, the actionable translation is that the delivery-and-dose system matters far more than which of two nearly identical precursors wins a message-board war

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HGF-MET signals via the MLL-ETS2 complex in hepatocellular carcinoma