Although narrowband UVB (NB-UVB) has replaced broadband UVB (BB-UVB) because of its greater effectiveness in dermatological phototherapy, it is twice as carcinogenic as BB-UVB at an equivalent inflammatory dose. To clarify the basis of the different genotoxicities, we comparatively evaluated the mutagenicities in mouse skin of the two UVB types along with their efficiencies in the formation of cyclobutane pyrimidine dimer (CPD), which is a major mutagenic DNA photolesion specifically produced by UVR. We found that the mutagenicity averaged per single molecule of CPD was 2.5- and 1.8-fold higher in NB-UVB-exposed epidermis and dermis, respectively, which indicates that NB-UVB is more mutagenic for the skin than BB-UVB at doses producing an equimolar amount of CPD. Analysis of effective wavelengths for UV photolesion formation with each UVB source revealed a remarkable difference in the peak effective wavelengths for CPD formation: 15 nm longer for NB-UVB in the epidermis. Although the analysis of mutation profiles showed largely similar UV-specific signatures between the two UVB types, a relatively stronger preference for UVA-specific mutations was observed for NB-UVB. These results suggest that the difference in the effective wavelengths for CPD formation leads to the different mutagenicities and carcinogenicities between the UVB sources.