TNF and Friedreich ataxia: Li et al. (69) provided further evidence for a role for TNF-α in the pathogenesis of FA by demonstrating that, while TNF-α initially inhibited the growth of HSCs from FA mice (Fancc−/−), longer-term exposure promoted the generation of cytogenetically abnormal clones that led to acute myelogenous leukemia upon transplantation into congenic wild-type recipients.