This difference could be explained by the association between nuclear IGF1R and HR DNA repair, and this hypothesis has been supported by numerous previous studies; i) the known association between HR deficiency and increased survival in these two tumor groups (by means of BRCAness/treatment responsiveness) [25–27], ii) IGF1R inhibition decreases HR DNA repair [28], iii) IGF1R and BRCA1 share a common function in the way they phosphorylate PCNA [29]; and iv) inhibition of BRCA1 makes cells more susceptible to IGF1R inhibition [12]. This evidence concerns the gene BRCA1 and neoplasm.