Of note, the correlation between IGF-1R overexpression and cancer development, as well as the role of its downstream signalling cascade, such as activation of the PI3K/Akt pathway, in the promotion of proliferation of breast cancer cell lines, have been reported in several studies.44–46 Dunn et al.47 also demonstrated that suppression of IGF-1R expression leads to inhibition of metastasis, invasion and adhesion of breast cancer cells.47 In this context, targeting IGF-1R appears to be a promising approach for inhibiting tumour growth and increasing therapeutic efficacy. The gene discussed is AKT1; the disease is breast cancer.