To the Editor.
—In their article in the March 1988 Archives, Hunter and colleagues1 state that "Attempts to elucidate the pathogeneses of these [genetic] subtypes have been confounded by studies that have considered all patients with RP [retinitis pigmentosa] as a single group," after which two RP studies of which I was one of the authors are referenced.It appears that a careful reading was not given to our articles, as Table 1 in the article on autoimmunity in hereditary retinal degeneration2 illustrates the great effort the UCLA Retinitis Pigmentosa Center takes to subdivide patients with RP on a hereditary and test rationale, while our study correlating the fluorescein angiographic findings with the presence or absence of antiretinal antibodies3 also looked at differences between patients with typical rod-cone vs cone-rod degeneration (type I vs type II RP, Baltimore classification). Hunter et al appear to be critical of