SNRK and neoplasm: At the molecular level, angiosarcomas show increased expression of the vascular-specific receptor tyrosine kinases, FLT1, TIE1, TEK, SNRK, and KDR, overexpression of the VEGF regulators HIF-1α and HIF-2α, amplified MYC in secondary angiosarcomas, recurrent angiogenesis-regulators PTPRB and PLCG1 mutations, FLT4 gene amplification in tumor with lymphatic differentiation, and, less commonly, CIC gene rearrangements in primary cutaneous angiosarcomas [1].