The 'road block' induced by the DNA damage to the transcription machinery triggers assembly of a transcription couple repair complex, whose composition and function are yet to fully understood. Damage recognition is achieved by the arrest of Pol II active complex. Subsequently various factors like CSA, CSB, TFIIH, XPG, XPF-ERCC1 complexes are recruited. The importance of active CSA and CSB are known from the mutation profile of the patients bearing the corresponding disease phenotypes. CSB can act as a 'repair-transcription uncoupling factor' that may use its DNA translocase activity to remove the Pol II activity from the lesion site. TFIIS may cleave up to 35 nucleotides from the 3' end of the nascent RNA product leading to the enhanced access to damage site on the corresponding template DNA.