We, therefore, examined the effect of ATM targeting on HNSCC and NSCLC CAF cultured ex vivo. We found that inhibiting ATM using KU55933 or shRNA knockdown, reverted CAF to a more quiescent phenotype, downregulating the expression of myofibroblast markers (SMA, collagen I, fibronectin; Fig. 3A–D), suppressing contractility (Fig. 3E) and inhibiting myoCAF-dependent cancer cell invasion (Fig. 3F and G). The gene discussed is FN1; the disease is cancer.