SummaryOverexpression of a pine MYB, PtMYB4, in Arabidopsis caused ectopic lignin deposition and allowed the plants to undergo photomorphogenesis even when they were grown in the dark. The phenotype caused by PtMYB4 overexpression was reminiscent of the previously characterised dark‐photomorphogenic mutant, de‐etiolated 3 (det3); consequently, we tested the hypothesis that MYB misexpression may explain aspects of the det3 phenotype. We show here that AtMYB61, a member of the Arabidopsis R2R3‐MYB family, is misexpressed in the det3 mutant. Semi‐quantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR) experiments suggested that AtMYB61 was misexpressed in a det3 background relative to wild‐type plants. Examination of AtMYB61 promoter activity in a det3 background showed that the spatial control of AtMYB61 expression was lost. In order to determine if such misexpression could explain the mutant phenotype, AtMYB61 was overexpressed in wild‐type Arabidopsis plants. Transgenic plants that overexpressed AtMYB61 had the same ectopic lignification and dark‐photomorphogenic phenotype as that of the det3 mutant. In order to test if AtMYB61 was necessary for these aspects of the det3 phenotype, AtMYB61 expression was downregulated in det3 plants in both antisense and sense suppression experiments. Suppression of AtMYB61 in a det3 mutant background restored all mutant phenotypes of the det3 mutant associated with development in the dark. Taken together, these results suggest that AtMYB61 misexpression was both sufficient and necessary to explain the ectopic lignification and dark‐photomorphogenic phenotypes of the det3 mutant.