Colorectal cancer (CRC) is one of the most frequent neoplasms and is responsible for the second highest mortality rate of all cancers in the more developed regions of the world. The molecular mechanisms of CRC are relatively well characterized and are correlated to the accumulation of genetic mutations and certain patterns of gene expression/over-expression. There are a number of possible molecular factors involved in CRC progression in the aforementioned pathways, which are as yet not well described. One of these factors appears to be the gene FJ 194940.1, previously termed P65. FJ 194940.1 consists of 6 exons and probably undergoes alternative splicing in malignant tissues. In this study, tissue samples from 102 patients with colon cancer were investigated to confirm alternative splicing and to correlate results obtained with clinicopathological parameters. A total of 18 splice variants, which arise from various combinations of 4 exons (II, III, IV and V) and exon-exon junctions between exons 1 and 2 (I/II); 2 and 3 (II/III); 3 and 4 (III/IV), as well as 4 and 5 (IV/V), were found. For statistical analysis the full length transcript was divided into parts A and B. Part A consisted of exons II and III, as well as I/II and II/III exon-exon junctions, whereas part B comprised exons IV and V, as well as III/IV and IV/V exon-exon junctions. The expression of part B of the FJ 194940.1 gene transcript is correlated with well-differentiated (G1) and moderately differentiated cases (G2). Lymphocytic tumor infiltration, a good prognostic factor in CRC, was significantly correlated to the presence of all elements in part A of the FJ 194940.1 gene transcript. Patients who had all elements in part A of the transcript survived for a shorter duration. Investigation of the FJ 194940.1 gene revealed that the gene had undergone alternative splicing. However, the role of its transcripts and potential proteins should be examined in detail.