An examination of the properties of T2 coliphage, after treatment with the nitrogen mustard di(2-chloroethyl)methylamine, revealed a remarkable similarity to those of T2 after X-irradiation. In particular, the phage remained capable of adsorption to the host cells and of combining with specific antibody, whilst showing a progressive loss of ability to kill the host cells with increasing dose. Further, a small degree of multiplicity and cross-reactivation was manifested, commensurate with that shown by phage X-irradiated in vitro. It is considered that these facts are consistent with the view that loss of plaque-forming ability is largely due to a failure of injection of the deoxyribonucleic acid moiety of the virus into the host cells following adsorption, an explanation already put forward by other workers in respect of X-rayed phage. This failure could arise by internal cross-linking of the DNA by the chloroethylamine, or of the DNA with the protein membrane. The experimental evidence supports the former proposal. The term 'radiomimetic' used in respect of di(2-chloroethyl)methylamine in the general title of this series is thus justifiable so far as phage inactivation is concerned.