Inhibition of IGF-1R abrogated rapamycin-induced phospho-Akt induction and substrate phosphorylation, and combination of rapamycin with an inhibitor of IGF-1R had additive effects on proliferation irrespective of PTEN status and increased apoptosis in a PTEN mutant cancer cell line (O’Reilly et al, 2006). The gene discussed is IGF1R; the disease is cancer.