Variations in the TrkAIII expression ratio to 18S rRNA, however, indicates that this relationship does not extend to MCPyV promotion of TrkA transcription, which suggests that TrkAIII involvement in MCC would be restricted to tumors exhibiting constitutive TrkA transcription, unveils a novel potential oncogenic post-transcriptional function for MCPyV large T-antigen in addition to inhibition of tumour suppressor activity [26] and is consistent with reports linking Alk and EGFR receptor tyrosine kinase oncogenes to MCC [3, 35]. Here, ALK is linked to neoplasm.