Firstly, the concentration of the endogenous IFNγ may be too low to stimulate the IFNγR; secondly, IFNγR is functionally inactive, as demonstrated in renal cell carcinomas (Dovhey and Ghosh, 2000); and, finally, STAT-1 lacks TGCT, as shown in pul-monary carcinoma and malignant melanoma cells (Kaplan et al, 1998; Lee et al, 1999). This evidence concerns the gene IFNGR1 and hereditary clear cell renal cell carcinoma.