They found that the expression of SRC-1 was relatively constant in mice with spontaneous prostate cancer, while that of SRC-3 was significantly increased; moreover, SRC-3 is overexpressed during prostate tumour progression in SRC-1-deficient mice, so SRC-3 may compensate for the loss of SRC-1 function [81]. The gene discussed is NCOA1; the disease is Familial prostate cancer.