~5of a given type, the continuous irradiation occurs over a constant time of exposure, but the dose rate (and the total accumulated dose in a given time) depend directly on the amoung of alpha emitter administered. Both dose and dose rate are relevant and important in internal alpha radiation induction of cancer. In the author's formula, if the only parameter that is varied is the dose rate (R), this would also vary the dose proportionally for a constant time of exposure. On this basis there is a direct relationship between incidence (or risk) and dose rate or dose size. Perhaps what the author intended, but did not make clear and explicit, was that the total dose should be kent constant by varying both the dose rate (R) and the time of exposure (t) such ‘that the product of the two (the total dose) would always be the same. Under these circumstances, as one increases the dose rate (R) one decreases the exposure time (t) proportionally, and the consequent reduction of the function t/T, reduces the value of R*t2(t/T¢) which is related to incidence or risk. However appropriate the use of the formula may be for estimating a two-mutation sequence from some kinds of radiation from external sources, it is artificial and neither appropriate nor realistic for tumor incidence or risk for continuous irradiation from internal alpha emitters which cannot be Limited to varying times of exposure in relation to dose rate, and it requires presumptions on the interrelationships among dose rate, time of exposure, total dose, relevant induction dose, and latent period in internal alpha radiation induction of tumors, as well as the assumption that a two-mutation sequence is, or is equivalent to, the mechanism of cancer induction.