Heterokaryon incompatibility (HI) is a form of nonself recognition during the formation of heterokaryons – cells containing genetically dissimilar nuclei. HI is controlled by het loci; of these, het-6 is a supergene complex encoding two tightly-linked incompatibility genes, un-24 and het-6, with allelic variants Oak Ridge (OR) and Panama (PA). het-6 encodes a HET domain protein with no known function outside of incompatibility, whereas un-24 encodes the large subunit of ribonucleotide reductase. Strains incompatible at het-6 can ‘escape’ from HI by mutation in the het-6 gene or suppress HI by mutation in vib-1, a transcription factor. This study examined the possible role of the het-6 promoter region in initiating escape, by introducing an ectopic het-6OR allele into a strain with a null endogenous het-6OR allele. Self-incompatible transformants exhibited delayed escape. A vib-1 mutant allele partially suppressed incompatibility at the ectopic het-6OR. This study provides insight into the process of escape.