By taking advantage of a genetic setting of PCa susceptibility in mice (prostate-specific Pten heterozygosity) [59], we demonstrated that transgenic Trib1 expression elicits a substantial increase in the incidence of PCa, thus providing unprecedented evidence in genetically engineered mouse models, to support the causal contribution of this pseudokinase to prostate tumorigenesis. The gene discussed is PTEN; the disease is posterior cortical atrophy.