Central to this mechanism is ITGα8's role as a specialized high‐threshold mechanoreceptor with distinct activation requirements—our hydrogel experiments demonstrate that ITGα8 exhibits preferential activation on substrates with specific elastic moduli, precisely matching the mechanical environment created by ADAMTS1‐mediated ECM remodeling.[49] This contrasts markedly with other integrin family members: ITGαv responds to low‐stiffness environments and mediates tumor invasion, while ITGα5 demonstrates broader stiffness responsiveness associated with general cell migration.[50]. The gene discussed is ADAMTS1; the disease is neoplasm.