The incidence of testicular germ cell tumors (TGCTs) has steadily increased to become the most common malignancy affecting men aged between 15-40 years. Seminomas and non-seminomas (embryonal carcinomas) comprise over 95% of TGCTs [1]. These are considered to arise in the testis from fetal germ cells that fail to differentiate correctly due to genetic and/or environmental factors. Although the exact mechanism is unclear, disruption of TGF-β superfamily signaling is implicated [2]. The well-characterized cell models of seminoma (TCam-2) and embryonal carcinoma (NT2/D1) were used to study the effects of TGF-β superfamily proteins activin A and BMP4 on TGCTs. Transcript changes were measured using RNA-sequencing and RT-qPCR following 6 hours of stimulation with activin A or BMP4. Major signaling pathways and biological processes affected were identified using DAVID analyses. Activin A significantly upregulated genes linked to pluripotency, cancer, TGF-β, Notch, p53, and Hippo signaling, whereas BMP4 altered TGF-β, pluripotency, Hippo and Wnt signaling components. Predicted key upstream regulators were identified using Ingenuity Pathway Analysis software and included pharmaceuticals. Reflecting the presence of both activin and BMP in the testis in vivo, we examined the potential for their crosstalk in TCam-2 cells using a dual promoter luciferase assay and documented a dose-dependent antagonism of BMP signaling by activin A. The importin protein, IPO5, levels and subcellular localization change dramatically in fetal and adult male germline cells [3], and IPO5 selectively mediates nuclear localization of the BMP-specific SMADs1/5/9 [4]. Here we show that IPO5 knockdown significantly impeded BMP4-induced transcription of BMP-regulated genes, providing evidence that IPO5 could play a crucial role in deciding which of the two arms of TGF-β signaling is more active in TGCTs. These results demonstrate how local activin A and BMP4 levels may modulate the TGCT transcriptome and could themselves be modulated to influence testicular cancer progression.