KRAS-driven tumours and B cell lineage tumours, such as multiple myeloma (dependent on clearing high levels of immunoglobulin), have been suggested (vide supra).1,20 It would appear, however, that malignant cells with high expression of an oncogene that drives high levels of protein synthesis would be a candidate as cells generally lack efficient mechanisms to curtail superfluous protein synthesis and are thus dependent on the proteasome/autophagosome to ride it of potentially toxic protein. The gene discussed is KRAS; the disease is AL amyloidosis.