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LIM domain binding protein 1 (LDB1) is a protein cofactor that participates in several multiprotein complexes with transcription factors that regulate mouse forebrain development. SinceLdb1null mutants display early embryonic lethality, we used a conditional knockout strategy to examine the role of LDB1 in early forebrain development using multiple Cre lines. Loss ofLdb1from E8.75 using Foxg1Cre caused a disruption of midline boundary structures in the dorsal telencephalon. While this Cre line gave the expected pattern of recombination of the floxedLdb1locus, unexpectedly, standard Cre lines that act from embryonic day (E)10.5 (Emx1Cre) and E11.5 (NesCre) did not show efficient or complete recombination in the dorsal telencephalon by E12.5. Intriguingly, this effect was specific to theLdb1floxed allele, since three other lines including floxed Ai9 and mTmG reporters, and a floxedLhx2line, each displayed the expected spatial patterns of recombination. Furthermore, the incomplete recombination of the floxedLdb1locus using NesCre was limited to the dorsal telencephalon, while the ventral telencephalon and the diencephalon displayed the expected loss ofLdb1. This permitted us to examine the requirement for LDB1 in the development of the thalamus in a context wherein the cortex continued to expressLdb1. We report that the somatosensory VB nucleus is profoundly shrunken upon loss of LDB1. Our findings highlight the unusual nature of theLdb1locus in terms of recombination efficiency, and also report a novel role for LDB1 during the development of the thalamus.