Although relevant small-molecule inhibitors have been extensively explored to dismantle self-defenses of tumors for improving therapeutic potencies14–16, such compounds still suffer from severe dose-limiting off-target toxicities owing to their indiscriminate suppression of stressfully overexpressed proteins in tumor and normally expressed proteins in healthy tissues that are necessarily involved in crucial intracellular events such as HSPs-assisted protein folding correction and TGFβ-mediated tissue repair3,8. The gene discussed is TGFB1; the disease is neoplasm.