RB1 and Merkel cell skin cancer: As discussed before, this view is sustained by (i) the mono-clonal integration of the viral genome within the tumor genome [7,38,39,40], (ii) the preservation of the RB1 interaction domain in the truncated LT [41], (iii) the transforming ability of the MCPyV TAs in vitro and in vivo [42,44,45], (iv) the dependency of established MCC cells on TA expression [42,43] and (v) the lack of recurrent mutations in established human oncogenes in virus-positive MCC [31,46,47] suggesting that there might be no crucial genetic contribution to oncogenesis other than MCPyV integration.