This activity was shown to be mediated possibly via an IGF-IR-independent and IR-independent mechanism, not only in the PCa cells PC-3 and LNCaP (Armakolas et al., 2010) but also in MG-63 osteosarcoma cells (Philippou et al., 2011) and in KLE endometrial-like cells (Milingos et al., 2010). Here, IGF1R is linked to posterior cortical atrophy.