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Mutations in the l(3)mbt tumour suppressor result in overproliferation of Drosophila larval brains. Recently, the derepression of different gene classes in l(3)mbt mutants was shown to be causal for transformation. However, the molecular mechanisms of dL(3)mbt-mediated gene repression are not understood. Here, we identify LINT, the major dL(3)mbt complex of Drosophila. LINT has three core subunits—dL(3)mbt, dCoREST, and dLint-1—and is expressed in cell lines, embryos, and larval brain. Using genome-wide ChIP–Seq analysis, we show that dLint-1 binds close to the TSS of tumour-relevant target genes. Depletion of the LINT core subunits results in derepression of these genes. By contrast, histone deacetylase, histone methylase, and histone demethylase activities are not required to maintain repression. Our results support a direct role of LINT in the repression of brain tumour-relevant target genes by restricting promoter access., Author Summary Mutations in the l(3)mbt result in the formation of brain tumours. The molecular basis underlying this phenotype has remained obscure. Here, we have isolated LINT, a novel protein complex containing dL(3)mbt, the corepressor dCoREST, and the uncharacterised protein dLint-1. We have used genome-wide ChIP–Seq analysis to map the binding sites of LINT. LINT occupies the promoters of many genes that are deregulated in l(3)mbt brain tumours, suggesting that these genes are repressed by LINT. Indeed, RNAi–mediated depletion of LINT subunits results in the derepression of these genes. Surprisingly, LINT-mediated repression is largely independent of histone modification status, arguing for a repression mechanism that operates by restricting promoter access.