IGF1R and neoplasm: As described by Villanueva et al., an increase in IGFR-1R and pAKT levels in a post-relapse human tumor sample is consistent with a role of IGF-1R/PI3K-dependent survival in conferring resistance to BRAFi and could be a plausible explanation of the death of BRAFi-resistant cells upon combined treatment with IGF-1R/PI3K and MEK inhibitors [67].