Benveniste’s experiments – known in the lay press as the “water memory” phenomenon – are generally considered to be a closed case. However, the amount of data generated by twenty years of well-conducted experiments prevents closing the file so simply. An issue, which has been little highlighted so far, merits to be emphasized. Indeed, if Benveniste failed to persuade his peers of the value of his experiments, it was mainly because of a stumbling block, namely the difficulty of convincingly proving the causal relationship between the supposed cause (“informed water”) and the experimental outcomes in different biological models. To progress in the understanding of this phenomenon, we abandon the idea of any role of water in these experiments (“water memory” and its avatars). In other words, we assume that “control” and “test” conditions to be evaluated were physically identical and differed only by their respective designations. We show in this article how simple probabilistic considerations allow to build a model that accounts for all aspects of Benveniste’s experiments. In this model based on probability amplitudes, constructive and destructive interferences emerge – or not – according to the experimental context. The recording of a statistical regularity shapes the intertwined whole constituted by the probability amplitudes of the states of the experimenter’s cognitive structures and of the experimental system. This model provides an alternative explanation to Benveniste’s experiments where water plays no role and where the place of the experimenter is central.

Epithelial–mesenchymal transition (EMT) is defined as a cellular process during which epithelial cells acquire mesenchymal phenotypes and behavior following the downregulation of epithelial features. EMT and its reversed process, the mesenchymal-epithelial transition (MET), and the special form of EMT, the endothelial-mesenchymal transition (EndMT), have been thought as a universal dogma controlling developmental and pathological processes. More than half a century of EMT study has made it a large research field and a mainstream concept. However, discrepancies and disputes over EMT and EMT research have also grown over time. Particularly, neither the epithelial and mesenchymal states/properties nor their regulatory networks nor specific markers have been defined, rendering the EMT, MET and EndMT concepts groundless. Moreover, EMT and MET effects should not be a cause, but rather a consequence of or an accompanying effect during developmental and pathological processes. EMT and MET represented by the change in cell shapes or adhesiveness or symbolized by EMT factors are biased interpretation of the overall change in cellular property and regulatory networks during development and cancer progression. The true meaning of EMT effects in some developmental and pathological processes, such as fibrosis, needs re-evaluation. But the core EMT factors are actually a few components of the regulatory networks of neural stemness, which determines tumorigenicity and pluripotency. The EMT effects in cancer progression and neural crest formation are wrong attribution of the role of neural stemness during cancer progression and the cell-intrinsic property of neural crest cells to the unknown mesenchymal state. It is time to reassess the significance of EMT and its related concepts in scientific research.