It is well known that the major histocompatibility system (MHS) has unique properties pertaining to antigenic strength (Démant, 1973). In the 1973 and 1975 Workshops we investigated alloimmune interactions to try to find out which MHS genes are involved and how they confer antigenic strength. We found that in several models therearespecial antigenic strength conferring and/or controlling genes, that there are probably several such genes unique for each model, situated throughout the mouse MHS (H‐2 complex). For example, the cell mediated lympholysis (CML) controlling genes, the Effector Cell Stimulating (ECS) genes, conferring strength against K and D region antigens are in the I region but separate from the I‐A Lad genes (Festensteinet al., 1974) while the allograft controlling genes, for various rejection models, are in the D region as well as the I region (Festensteinet al., 1975). This is an attempt to bring together the data from these various models to formulate a functional concept of antigenic strength, in relation to its genetic b