Previous studies have shown that GLI2 becomes constitutively active in concomitance with the loss of PC, even accelerating tumor formation.[31] To examine whether PC disassembly influences GLI2 activation, we treated iHOKs with a non‐toxic dose of tubacin (Figure S4A, Supporting Information), a selective inhibitor of α‐tubulin deacetylating activity of Histone deacetylase 6 (HDAC6) without affecting histone acetylation, gene expression, or cell cycle,[32] to protect cells from HDAC6‐mediated PC resorption under high stiffness conditions. The gene discussed is GLI2; the disease is neoplasm.