Connective tissue morphogenesis has long been interpreted through a fibroblast-centric paradigm, yet this view contains a fundamental spatial paradox: it requires localized cells to perform global geometric planning without any mechanism to perceive large-scale tissue axes. I propose the Poisson-Press Theory, a physically grounded model in which anomalous Poisson compression and poroelastic syneresis act as the primary macromechanical generators of planarization, alignment, and lamination. This restores the correct causal hierarchy: physics establishes the geometric template, and biology consolidates it. Growth-induced tension—arising from the geometric mismatch between volumetric expansion (∝r³) and surface area (∝r²)—creates obligatory orthogonal Poisson compression in hydrated collagen networks. This compression expels interstitial fluid, collapses porosity, and forces fibers into planar, directionally aligned configurations. Under different boundary conditions, the same physical mechanism produces distinct fascial architectures, from epidermal–subcutaneous planarization to cylindrical Poisson collapse in the transversalis fascia and pure compressive welding in the retroperitoneal fascia. A natural subtraction experiment using CT scans of congenital unilateral renal agenesis demonstrates that the parietal lamina of the posterior renal fascia forms autonomously at its predicted anatomical position despite the lifelong absence of organ-dependent hoop stress, confirming a system-level mechanical origin. From an evolutionary perspective, human-specific front-loading of truncal stiffening concentrates fetal movement energy into multi-axial tension fields, intensifying Poisson compression at mid-gestation. The same principles extend into adult life, reframing occupational and athletic remodeling as continuous adaptive mechanomorphogenesis driven by persistent Poisson-Press fields.