Abstract: Objective To investigate the effect of the JAK family member Tyk2 on androgen receptor (AR) phosphorylation and the proliferation of prostate cancer cells. Methods LNCaP and LAPC-4 cell lines as subjects, without androgen settings, after epidermal growth factor (EGF) stimulation, giving AIM-100/Baricitinib (INCB 028050) management, immunoprecipitation and/or western blot was used to observe AR phosphorylation. RNA interference targeted silence Tyk2 gene was transfected into LNCaP and LAPC-4 cell lines. Western blot was used to observe the effect on AR phosphorylation. CCK-8 was used to measure cell proliferation. Results EGF can induce AR phosphorylation at Tyr-267 and proliferation of prostate cancer cells (P <0.05). AIM-100 inhibited the proliferation of prostate cancer cells (P <0.05), and AR Tyr-267 phosphorylation mediated by Ack1 and Tyk2. However, INCB inhibited Tyk2 phosphorylation and AR Tyr-267 phosphorylation, as well as the proliferation of prostate cancer cells (P <0.05). Conclusions The JAK family member Tyk2 played a critical role in facilitating EGF-induced AR site-specific phosphorylation at Tyr-267 and in promoting prostate cancer cell proliferation.