There is emerging evidence that genomic and chromosomal instability are features of CTCL, including variants such as MF, Sézary syndrome, and primary cutaneous CD30+ LCAL, and that specific chromosomal abnormalities are common. Additional resolution of specific regions of chromosomal loss and gain are required to define putative genes that may be of fundamental pathogenetic importance in CTCL. Inactivation of well-defined cell cycle and TSG are common as for other types of NHL. The prognostic significance of these abnormalities in CTCL has yet to be determined. The dysregulation of specific transcription factors is of interest, but requires further study. It is hoped that greater understanding of these molecular abnormalities will permit the development of CTCL-specific therapies that alleviate suffering and prolong survival.