In Hodgkin’s lymphoma, CD99 induced the loss of multinucleated Reed–Sternberg cells morphology and redifferentiation [84] by regulating the expression of SEPTIN2, a member of the septin family that is involved in cell polarity and regulation of the actin and tubulin cytoskeleton (for a review see [89]), and STATHMIN, a cytoskeletal protein that is overexpressed in several malignancies and plays a significant role in cell differentiation [90], including B cell differentiation [91]. This evidence concerns the gene CD99 and Hodgkins lymphoma.