  As a consequence of this heterogeneity, SLI, researchers have  introduced a number of subtypes of the disorder, including such  things as ‘Verbal auditory agnosia,’  ‘Lexical-syntactic deficit syndrome’ and  ‘Phonological programming syndrome’ (Bishop 1994). Also  as a consequence, and in part because studies do not always  distinguish between different subtypes, the etiology of SLI in  general is not well understood (O'Brien et al. 2003), although  recent research suggests at least two distinct genetic loci are  involved in at least some subtypes of the disorder (Bishop 2006).  Some posit an underlying defect in the ‘grammar module.’  For instance, Rice and Wexler (1996) attribute SLI individuals'  morphological deficits to a missing UG principle, namely, the  principle of inflection, and Van der Laly and Stollwerk 1997,  attribute some SLI children's difficulty with anaphora to their  failure to acquire Binding Theory. Others see non-linguistic defects, such as auditory, memory or processing deficits as the root problem.  For instance, Tallal 1980, 1985 argue that many SLI cases result  from deficits in the processing of rapid auditory stimuli, giving  rise to a failure to learn to distinguish phonemes correctly, which  in turn leads to a failure to acquire other aspects of grammar.  Others, such as and Norbury, Bishop and Briscoe 2002 argue that such  children's limited processing capacities are the culprit.