As our results suggest JUN-dependent activation of the IL-6/STAT3 axis and our previous study connected loss of activated STAT3 in Pten-deficient PCa to increased tumor burden via disruption of senescence [12], we sought to analyze STAT3 tyrosine 705 (Y705) phosphorylation (pSTAT3Y705) in the Jun-deficient background. The gene discussed is IL6; the disease is neoplasm.