Since the reporting of clinical improvement observed in the treatment of psoriasis with aminopterin,1 our interest has been aroused to reevaluate the results obtained with this drug as well as with its close relative amethopterin. These drugs were used in our private practice in relatively low but therapeutic dosage. These folic acid antagonists are known2 to inhibit proliferation of connective tissue, anomalous and undifferentiated cells, and epithelial cells. By successfully competing with their analogue, folic acid, they interfere with the conversion of folic acid to the citrovorum factor which is important in the biosynthesis of nucleic acid components necessary in the development of epithelial cells. It has been shown that histologic response2 to aminopterin therapy of psoriatic lesions consists of reduced hyperkeratosis, parakeratosis, and acanthosis which parallel the observed clinical improvement in the psoriatic lesions. The very nature of the action of amin