Abstract: The neural mechanisms of interval timing are not well understood. Language disorders provide a window for the search of the genetic basis of verbal communication which support the perception and execution of interval timing. Here we focus on the performance of a subject, A, with a chromosomal translocation t[7;11][p13;p13] along with a pericentromeric inversion with rupture points in 7p13 and 7q31, the latter being the locus of FOXP2. It was found that A significantly underperformed in a comprehension test with basic grammatical constructions compared to a Spanish population matched for age. It was also found that A underperformed in this perceptual test in both varieties compared to a control matched for age, sex, speech varieties, schooling and socioeconomic background. We found that there is a statistically significant correlation between A’s failure in understanding and the presence in the auditory stimulus of an interval in the range of 20-200ms, which happens to be crucial for the specific integration of longer intervals of the utterance. These findings are coherent with studies which suggest that the modulation of timing is supported by a functionally integrated network involving the striatum, thalamus cortex and cerebellum, where FOXP2 is expressed.