A substantial population of children and adolescents struggle with reading comprehension despite adequate phonemic decoding (word-level reading) and intellectual ability. Individuals with this pattern of performance are considered to have specific reading comprehension deficit(S-RCD).Despite two decades of study on the profiles of behavioral performance associated with S-RCD, there is no current consensus on the causal mechanisms of the disorder. Recent progress in identifying such mechanisms includes studies that have utilized comprehension age match and longitudinal designs which have identified several comprehension subskills that are predictive of S-RCD development. However, disagreement persists over which deficits are core to S-RCD, which are comorbid and which are simply a consequence of poor comprehension. Further, almost no research on this disorder has sought to identify neurobiological endophenotypes that may enhance our understanding of causal mechanisms. Here, we offer a review of the literature on core language and higher-level language deficits associated with S-RCD, including studies that examine the neurobiological basis of this disorder. What emerges is a relatively consistent pattern of subclinical impairments across a range of comprehension subskills that may put pressure on the complex process of reading comprehension. These subskills include semantic and grammatical processing, inference making, and other higher-level language skills such as comprehension monitoring. This disorder also appears to have a neurobiological basis, though further study is needed to establish the precise disruption in neurocircuitry. Suggestions for further research include the continued use of online, temporally-sensitive measures such as eye-tracking and event-related potential, additional studies of the neurobiology of the disorder, as well as longitudinal tracking and identification of early behavioral and brain markers for S-RCD prior to formal schooling.