Fifteen quantitative trait loci (QTL) for cell wall digestibility and lignin content were shown in the recombinant inbred line (RIL) progeny descended from the cross between F288 and F271, two early dent lines of contrasted cell wall digestibility. Among these QTL, those located in bin 6.06, respectively explained 20 and 40% of the phenotypic variation for lignin content and cell wall digestibility. Expression of genes related to cell wall and lignin biosynthesis was investigated with the "MaizeWall" macro-array in two RIL having favorable alleles for low lignin content and high cell wall digestibility, except in bin 6.06 where RIL39 and RIL99 had unfavorable and favorable alleles, respectively. In the lignin pathway, three PAL, 4CL1, ZmCCR1, COMT, and ZmCAD2 genes were under-expressed in RIL99 in comparison to RIL39. In addition, two cytochrome P450, ZmCHS, and ZmCHI1 genes were simultaneously under-expressed while F5H2 and two OMT ZRP4-like genes were over-expressed. However, none of these genes were mapped in bin 6.06. Based on maize-rice synteny and on Maize Genome Sequencing Project data, several putative candidate genes related to lignin content and lignified tissue patterning were found in the support interval of bin 6.06 QTL. These genes included one C3'H which is likely the missing constitutive gene of the maize lignin pathway. Three ZRP4-like OMT were also shown in the support interval of the QTL. However, their involvement in the lignin pathway has not yet been firmly established. Several regulation or transcription factors were also shown in the QTL support interval. Among them, MYB, zinc finger, bZIP, and COV1 genes belong to families with members involved in lignification regulation or in lignified tissue patterning. In addition, auxin response factors have been shown to be indirectly involved in plant lignification. Moreover, several genes encoding proteins of unknown function and genes annotated "retrotransposon-like" were also located in the QTL support interval. Current results are not conclusive on the candidate gene discovery, but strengthen the hypothesis that regulation genes are better candidates than genes involved in the monolignol pathway. Fine mapping, association genetics, and/or functional validation have to be considered for more definite conclusions.