RTK-targeted cancer therapies are compromised or limited when tumour cells circumvent the action of a single agent, and multiple agents due to the readjustments in coexpression of HER2/HER3 receptors, their ligand binding dynamics, or changing preference for the dimerizing partner [17, 21, 61, 74, 75] suggest that the anticancer effect of these agents might be further optimized or be better predicted by effectively limiting HER2/HER3 expression at the DNA level or at least identifying a common regulatory centre of HER2 and HER3 transcription. This evidence concerns the gene ERBB3 and cancer.