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We were impressed by the similarity and complementarity between experimental results concerning neurotoxicity induced by prefibrillar oligomers (PFOs) of two different proteins belonging to the “amyloid” family: salmon Calcitonin (sCT) and Amyloid-β1-42 (Aβ1-42). The results were recently published by our group for sCT [1] and by Yasumoto’s group for Aβ1-42 [2]. The comparison is very interesting in the open debate about the intriguing hypothesis of the existence of a “common mechanism” in the pathogenesis of amyloid neurodegenerations. Here we wrote a comment to analyze in detail this parallelism and to suggest a possible interpretation. Briefly, the existence of a “common hydrophobic profile” in the central parts of the primary sequences of the two proteins could lead to the formation of metastable PFOs characterized by a “common hydrophobic outfit” able to damage neurons via a “unified mechanism” we proposed for sCT where “membrane permeabilization” and “receptor-mediated” paradigms coexist.