Whether a gene is ready for action or not depends on a process called chromatin remodelling. If the gene’s DNA is relaxed, it is ready for action. If it is ‘tense’ and tightly coiled on the structures that support it (histones) then the proteins necessary for reading and making the gene’s product just can’t get to their work stations to kick start the gene.

You can relax genes using an epigenetic tag called acetyl. This requires enzymes called Histone Acetyl Transferases (HATs) - an example is CBP. Jefferies’ team couldn’t find anything obvious at fault with the TAP gene, but spotted that the level of acetyl affected the amount of TAP protein in the cell. This seems to be true for ovary, prostate, skin, cervix, breast and lung cancer. Too little acetyl means low levels of TAP and loss of the one-of-us ID. But low TAP wasn’t a result of too little CBP to add the acetyl. The enzyme just got lazy.

In the world of cancer biology research, merely finding a mechanism that brings about the change from normal to abnormal is a triumph. Finding a way to fix the fault often comes much later. But Jefferies’ group came up trumps because they found a way to turn the TAP back on and flush cancer out of hiding.