In particular, the d16HER2 splice variant, which is expressed as a proportion (approximately 2–9%) of WTHER2 in human HER2-positive BC18,19, may have a crucial pathobiological role given that the post-transcriptional loss of 48 nucleotides in the extracellular domain induces the formation of stable and constitutively active HER2 homodimers on the tumor cell surface18,20. Here, ERBB2 is linked to neoplasm.