Abstract
Elucidating the molecular and genetic basis of a hereditary disease often has implications that go beyond the understanding of the disease itself and that may concern important biologic processes. When it was shown that a form of primary immunodeficiency, major histocompatibility complex (MHC) class II deficiency (also referred to as the bare lymphocyte syndrome), was in fact a disease of gene regulation involving trans-acting regulatory factors,1 there was hope that elucidating the genetic basis of that rare disease might lead to the identification of the essential regulators of MHC class II gene expression. MHC class II genes, originally described . . .