One possible explanation for the lack of effects of stathmin absence during mouse carcinogenesis could reside in compensatory overexpression of other members of the stathmin family, namely SCG10 (Superior Cervical Ganglia 10, also known as stathmin 2), SCLIP (SCG10-like protein, also known as stathmin 3) or RB3 (also known as stathmin 4) [46]. This evidence concerns the gene STMN2 and cervicitis.