The study by Earl P. Benditt and John M. Benditt investigates the origin of human atherosclerotic plaques, focusing on whether they are polyclonal or monoclonal. Using the X-linked glucose-6-phosphate dehydrogenase (G6PD) enzyme in heterozygous females, they analyzed 30 plaques from 59 samples of normal aorta and iliac artery walls from four females. The results show that fibrous caps of relatively large plaques (0.5 cm or more) are composed of cells producing a single or predominantly one enzyme type, while smaller samples (0.1 mm²) of artery wall media and intima are composed of a mixture of cell types. This suggests that atherosclerotic plaques are monoclonal, likely due to mutation caused by chemical mutagens or viruses. The study challenges the traditional injury-repair hypothesis and supports the idea that atherosclerosis may result from cell transformation rather than a response to injury. The findings also highlight the importance of considering factors that can transform cells, such as chemical mutagens or viruses, in the etiology and pathogenesis of atherosclerosis.The study by Earl P. Benditt and John M. Benditt investigates the origin of human atherosclerotic plaques, focusing on whether they are polyclonal or monoclonal. Using the X-linked glucose-6-phosphate dehydrogenase (G6PD) enzyme in heterozygous females, they analyzed 30 plaques from 59 samples of normal aorta and iliac artery walls from four females. The results show that fibrous caps of relatively large plaques (0.5 cm or more) are composed of cells producing a single or predominantly one enzyme type, while smaller samples (0.1 mm²) of artery wall media and intima are composed of a mixture of cell types. This suggests that atherosclerotic plaques are monoclonal, likely due to mutation caused by chemical mutagens or viruses. The study challenges the traditional injury-repair hypothesis and supports the idea that atherosclerosis may result from cell transformation rather than a response to injury. The findings also highlight the importance of considering factors that can transform cells, such as chemical mutagens or viruses, in the etiology and pathogenesis of atherosclerosis.