Several mechanisms underlying cancer resistance in NMRs have been also reported, including hypersensitivity to contact inhibition (early contact inhibition)7, secretion of high-molecular-mass hyaluronan8, triggering apoptosis or senescence when either p53 or Rb tumour suppressors is inactivated7,9, high levels of p5310, and overregulation of telomerase activity11. The gene discussed is RB1; the disease is neoplasm.