We previously showed that active Src is localised to intracellular puncta containing autophagy proteins in FAK -/- SCC cells, allowing FAK-deficient cancer cells to cope with high levels of ‘untethered’ active Src (and other FAK-interacting tyrosine kinases, e.g. Ret) (Sandilands et al., 2012a, 2012b). The gene discussed is RET; the disease is cancer.