Likewise, the different strategy used for eliminating the suppressor function of TP53 (expression of a defective TP53‐ER fusion protein rather than the total genetic inactivation of the Trp53 gene) has enabled us to generate a model that does not have the high basal levels of tumour formation that are usually driven by the full Trp53 knockout condition. Here, ESR1 is linked to neoplasm.