This paper reports the surprising finding that selection for suramin resistance in the bloodstream form of Trypanosoma brucei rhodesiense results in a breakthrough population expressing a particular variant surface glycoprotein (VSG). The authors ruled out the possibility that a switch to this VSG also involved co-expressed genes in the VSG expression site, i.e. expression site switch, by demonstrating that the sequence of ESAG 7, one of the expression site-associated genes, remained unchanged in trypanosome populations before and after suramin selection. Moreover, replacement of the original VSG reversed suramin resistance. The authors point out the folly of this resistance mechanism for a trypanosome reliant on switching VSG for its long-term survival in the mammalian host -- an effective immune system will destroy a trypanosome that always expresses the same VSG.