Trypanosoma brucei is an extracellular pathogen that evades the host antibody response through antigenic variation of its variant surface glycoprotein (VSG) coat. It has long been believed that this immune evasion is achieved primarily by replacing the expressed VSG coat with a completely distinct antigen, resulting in complete immune evasion. However, recent evidence suggests that the parasite preferentially diversifies expressed VSGs by introducing small sequence changes through recombination. These modifications appear to accumulate until complete immune evasion is achieved. In this opinion article, we propose that the concepts of antigenic drift and shift, commonly used in the field of influenza research, apply well to antigenic variation in T.brucei and better reflect the complex nature of immune evasion in this pathogen.