Taken together, it is tempting to speculate that the mechanism of RSZ breakage and that of CFS expression, at least for those that are sensitive to the loss of ATR or ATM functions [12], [13], might be conserved and that the mammalian Top2 and condensin may similarly play a role in promoting fragile site expression. The gene discussed is TOP2A; the disease is myalgic encephalomeyelitis/chronic fatigue syndrome.