- 16 isoenzyme cell types of the female but from a single transformed cell, In this latter context they stated that the mechanism compatible with the monoclonal nature of atherosclerotic plaques is mutation, and that the likely causes are chemical mutagens or viruses. All that the actual data (isoenzyme data) in this paper (Benditt and Benditt) really show is that the plaques arise solely or predominantly from one or the other of the two embryonically determined isoenzyme cell types, with differentiation or metaplasia of the cells of either type in certain characteristic ways under the atherosclerotic circumstances, and not that plaques necessarily had origin from single (versus multiple) cells of the isoenzymecell type predominating. The actual data did not show thet cell mitation was involved, as is stated by the author of the present document under review. Nor does proliferation of a mutated cell necessarily result in a tumor. " Benditt and Benditt acknowledged the possibility that the reason for the sole or predominant presence of one or the other of the two Lsoenzyme cell types in the plaques is not a monoclonal origin but rather some process selecting from one or the other of the two cell types. _Benditt and Benditt did not actually define the atherosclerotic plaque as an arterial tumor as the author of the document under review seems to imply in relation to his reference to the paper by Benditt and Benditt. Page 11, lines 3-4 - "Elkeles(“1,43) has observed anomalously high concentrations of alpha activity at the calcified plaque sites." Comments: Elkeles (19°64) (author's reference+2) pointed out the well known fact that calcium deposition in various soft tissues is a manifestation of aging. Elkeles referred to a paper by Blumenthal et al. who micro- incinerated human aortas and showed that calcium was deposited in the