In human breast cancer cells, upregulation of IGF-1R expression was reported to resist anoikis by inhibiting activation of p53 and p21 [51], and IGF-1R/Akt signaling promoted LIP expression to inhibit anoikis [52], and IGF-1R mediated Akt activation through RACK1 to promote anchor growth of breast cancer cells [53]. The gene discussed is AKT1; the disease is breast cancer.