Sequence-directed bending is an alternative conformation of the DNA molecule determined by regions containing blocks of 2 or more dA/dT tracts repeated for each ~10 base pairs or multiples of them. These tracts promote a deflection on the helix axis of the double helix from straight line. Bent DNA molecules can be identified from an abnormal polyacrylamide gel migration and have been found in association with promoters regions, MARs (Matrix Attachment Region), replication origins, intronic segments, etc. In our laboratory we have mapped intrinsic bending DNA sites in the AMPD2 gene (Adenylate deaminase 2) amplicon, which contains the GNAI3, GNAT2 and GSTM4 genes and a zone of replication initiation, oriGNAI3, and other potentially replication sites – oriA, oriB and oriC. In the current work, a partial sequence of the GNAT2 gene that includes the third to sixth introns and exons was analyzed. Our objective is to screen the bent DNA sites on this gene segment, especially in intronic sequences. These bent DNA sites were identified by the electrophorectic behavior of restriction fragments in agarose and polyacrylamide gels and also by computational predictions and modeling using Map15a and 3d15m1 software. After electrophoresis, an R-value (ratio between the real and the apparent molecular size observed in polyacrylamide gels) was calculated. The 377 bp fragment that includes intron 3 and 129 bp of the exon 4, showed the slower mobility in polyacrylamide gels (centralized bent DNA site) with R-value 1.13. The enzyme restriction fragments with 1139 bp and 1146 bp have shown fast mobility in polyacrylamide gels (decentralized bent DNA sites), R-values 0.85 and 0.80, respectively. The first of these fragments includes the exon 4 and the introns 3 and 4. The fragment with 1146 bp has the exons 5 and 6 and the introns 4, 5 and 6.  The ENDS ratio analysis showed a peak of 1.16 at the intron 3, which indicates intrinsic curvature. The 2D modeling of these fragments showed a curved structure in all of them and allowed the identification of bent sites position involved in the abnormal migration. Further analysis should be necessary for the study of the functional role of the bending sites in intron segment of the GNAT2 gene in the AMPD2 amplicon.