The authors demonstrated that breaking the stress response loop (by depleting HSF1 or P23, a protein that helps to activate it, or inhibiting HSF1) reduced the chronic activation of HSF1 in cystic fibrosis cells, increased the levels, stability, and trafficking of mutant CFTR protein, and, crucially, increased its chloride channel activity in the membrane—the very activity whose absence is responsible for the disease symptoms. The gene discussed is CFTR; the disease is cystic fibrosis.