Introduction: Duchenne/Becker muscular Dystrophy (DMD/BMD) is the most common hereditary miopathy in the human populations. It is characterized by a muscular progressive weakness that causes, for the Duchenne type, the death of the patient for cardiac and / or respiratory fault during the second decade of his life. For the Becker type, the muscular alterations are less severe and the patients generally survive up to the adult age. The DMD gene, responsible of the disease, is located in the short arm of the chromosome X and is inherited in recessive form joined to X chromosome. Identificación de mutaciones y diagnóstico molecular de portadoras en familias mexicanas con distrofia muscular Duchenne/Becker Revista Electrónica Nova Scientia, Nº1 Vol. 1 (1), 2008. ISSN 2007 - 0705. pp: 136-149 - 139 - The genetic deletions of some parts of DMD gene are the most frequent mutations associated with the disease. Due to the absence of clinical manifestations in the possible carriers, the identification of them only could be realized by means of molecular studies. In the present work we studied the distribution of genetic deletions in the DMD gene of Mexican patients with DMD/BMD and in women who belonged to Mexican families with past history of the miopathy, the carrier status was determined. The patients and your relatives used in this study were not studied before. Method: We obtained DNA and RNA of peripheral blood lymphocytes of patients with DMD/BMD and women in risk, who belong to Mexican families with past history of the disease. The concentration and integrity of the nucleic acids were determined with spectrometry and electrophoresis in agarosa gels. The genetic deletions were identified by multiplex amplification of the two hot spots mutations sites and promotor region of DMD gene. The carrier diagnosis was made by genetic linkage using 5 microsatellites located in the DMD gene. In the families where the genetic deletion was identified, the diagnosis of carriers was made by RT-PCR. Results: The deletions were identified in 8/23 patients. In four of them, the extension of the deletion was delimited. In one patient the deletion affected two nearby genes, GK and DAX-1. An alternative splicing was identified in a patient, which would explain the slight phenotype that he presents. With linkage genetic and RT-PCR studies, 6/10 women were carriers. Discussion: The percentage of deletions in our patients was minor to the reported in other populations. Other studies are necessary to do with a greater number of patients, for to know if this low frequency is typical of our population. The use of genetic linkage and RT-PCR studies increase the possibility to define the carrier status in Mexican women belonging to families with past history of the disease. With these studies we can offer them a genetic council suitable. This one is the first work done in Mexico in which the diagnosis of this myophatia was done by RTPCR, is the first time in which a Mexican DMD patient, with continuous genes Syndrome, was characterized at molecular level, and we identified an alternative splicing in one patient with an atypical phenotype