Klebsiella pneumoniae is a Gram-negative bacteria responsible for causing a variety of infections, such as pneumonia, hepatic abscess, meningitis, urinary tract infection among others. In recent years, an increase in resistance to antibiotics has been observed for some strains of K. pneumoniae. In addition, increasing cases of severe infections in healthy subjects have emphasized the importance of studying the mechanisms of virulence that determine the pathogenicity of K. pneumoniae. The communication between bacteria denominated quorum-sensing is an important mechanism of virulence factors. This communication happens through self-inducers molecules codified and captured by luxS/luxI and luxR, respectively. Another important component responsible to regulate the expression of innumerate virulence factor pathogenic bacteria is the iron. This regulation is mediated by the Fur transcriptional regulator which, when complexed to iron, binds to specific sequences, called Fur boxes, located in the promoter region of the target genes, leading to the repression or induction of the transcription of these genes. Bioinformatics analyses were used to identify genes homologous to luxR genes in the K. pneumoniae genome. For these analyses the nucleotide and amino acid sequences of the luxR genes of other Gram-negative bacteria were used. Identification of the homologous genes was performed on the genome of K. pneumoniae MGH78578 annotated in the NCBI, using the NCBI BLAST program. Moreover, genes homologous to luxR identified had their promoter region searched for the identification of probable Fur boxes. The results showed eight homologous genes to luxR, besides the already known sdiA. The amino acid sequences of the proteins encoded by genes homologous to luxR indicate helix-turn-helix (HTH) DNA binding domains, which are typical of LuxR-type regulators. In addition, Fur boxes were identified in the promoter or inside region these homologous, as well as in sdiA and luxS gene, identified. These results reveal the possibility of the quorum-sensing mechanism being regulated by iron levels in K. pneumoniae.