This thesis explores cancer and immune system mechanobiology, while considering actin cytoskeleton remodeling as a potential immune evasion strategy. Similarly to the now widely accepted concept of immunosurveillance, the role of cellular mechanical properties in cancer progression ran into controversy at first. However, the discovery of a positive correlation between extracellular matrix stiffness and tumor phenotype has lastingly marked cancer mechanobiology as a promising field of study. Over time, researchers' interest has encompassed cell stiffness determining factors and their significance in immune synapse. During metastatic cascade, cancer cells undergo changes in morphology and elastic properties. This is primarily caused by actin cytoskeleton dynamics. Spreading of cancer cells across the perivascular niche is characterized by an increase in myocardin-related transcription factor (MRTF) signaling. This increases the amount of cellular actin filaments, which then assemble into stress fibers, thus increasing cellular stiffness. The increase in stiffness makes cells more stimulatory to lymphocytes and therefore more susceptible to elimination. Since the afforementioned step is crucial in the metastatic cascade, cancer cells need to finely regulate MRTF signaling in order to successfully avoid elimination and form colonies. Tumor cell actin response has been suggested as an alternative evasion mechanism, however its details remain elusive.