Human induced pluripotent stem cell derived endothelial progenitors (hiPSC-EPs) undergo vasculogenesis, the self-assembly of cells into vascular lumens, but unlike functionalized endothelial cells, the mechanobiology of this process has not yet been well characterized. Detailed understanding of this process will be critical to development of effectively vascularized therapeutic tissue constructs [1]. We have recently developed an integrated 3D traction-force-microscopy finite-element inverse-modelling pipeline that determines cellular traction forces and additionally heterogeneous mechanical properties around cells associated with extracellular-matrix (ECM) deposition and matrix-metalloproteinase degradation [2]. Application to hiPSC-EPs revealed cell-induced changes in hydrogel modulus ranging 3 orders of magnitude [3]. Presently, we shifted focus to the cytoskeleton within hiPSC-EPs and developed a second inverse modelling step to determine internal actinomyosin stress-fiber orientations and force-generation levels. 3-D imaging of hiPSC-EPs and surrounding hydrogel-embedded fiducial-marker displacements between relaxed and contractile states allowed creating realistic cell meshes. Our first inverse-modelling step reconstructed heterogeneous hydrogel moduli across orders of magnitude by minimizing displacement mismatch with Tikhonov regularization. Numerical stability with our large-deformation hyperelastic material model was achieved by accounting for compressible behaviours in the hydrogel and prescribing an exponential relationship between the control variables and modulus [3]. Next, we substantially improved and applied a previously developed, second inverse-modelling step [4] to determine cellular stress-fiber architecture. The stress-fiber inverse model was applied in two variants: a single-fiber representation and a novel fiber-dispersion representation of force generation. Spatially varying fiber orientations and forces within hiPSC-EPs were significantly different between single and cluster specimens; cell-cell junctions produced signature fiber-orientation and dispersion patterns. Cellular protrusions near deposited ECM exhibited high force generation. Endothelial-cell vasculogenesis initiates with fast single cells and subsequently slow clusters with increased integrin junctions [5]. Our findings suggest hiPSC-EPs increase force generation in their own second stage to support movement against increased adhesion to ECM.