Thymic epithelial tumors (TETs), including thymomas and thymic carcinomas (TCs), are rare neoplasms comprising 0.2–1.5% of malignancies, characterized by heterogeneity in clinical behavior and molecular features. The Hippo signaling pathway, a key regulator of cellular proliferation and differentiation, has been implicated in TET progression, yet its precise role remains unclear. This study investigates the expression and regulation of core Hippo pathway components—YAP1, TAZ, SAV1, MOB1, LATS1, MST1, and TEAD4—in TETs through an immunohistochemical analysis of 77 samples. MOB1 and SAV1 were consistently expressed across all TET subtypes, suggesting stable Hippo pathway activity. MST1 showed low to moderate expression, with higher levels in TCs. LATS1 exhibited very strong expression in TCs and moderate to strong levels in other subtypes. TEAD4 displayed variable expression, being stronger in TCs. TAZ expression showed marked variability in A-B3 thymomas, while TAZ was nuclear negative in most B1-B3 thymomas but strongly expressed in the cytoplasm. In contrast, TAZ in TCs was predominantly cytoplasmically negative and showed little nuclear expression. YAP showed weak to moderate nuclear expression in A-B3 thymomas but was largely absent in TCs, with occasional cytoplasmic positivity. The findings indicate the differential regulation of the Hippo pathway across TET subtypes. The OFF state of the Hippo pathway in thymoma A may allow for "controlled" proliferation, supporting homeostasis without aggressive behavior. In contrast, TCs exhibit complex Hippo pathway dysregulation. The moderate to strong expression of TAZ, MST1, LATS1, and TEAD4 in TCs suggests a mechanism where TAZ substitutes for YAP, promoting pro-oncogenic TEAD4-mediated signaling, potentially driving uncontrolled proliferation and tumor progression. This highlights the potential involvement of other pathways or epigenetic factors in TCs. Further validation through Real-Time PCR and Next-Generation Sequencing is needed to confirm these findings, identify mutations, and uncover the mechanisms underlying TET tumorigenesis. These insights may inform therapeutic strategies targeting the Hippo pathway in TETs.