In this situation, the displacement of KANK1 from FAs and CMSCs may cooperate with the biomechanical signals from the tumor environment via destabilizing microtubules and activating RhoA leading to stress fiber formation and myosin II activation, and enhancing the actomyosin-Talin linkage and force transmission across integrins leading to adhesion strengthening and enhanced tumor cell migration and invasion. Here, KANK1 is linked to neoplasm.