Given human wild-type SH3BGRL was shown as a tumor repressor in a breast cancer cell line by inactivation of FAK-Src pathway [10], we examined the Src activation situation and the downstream AKT and MAPK signaling pathways and observed that knockdown of SH3BGRL evidently activated Src as well as the downstream PI3K-AKT and MAPK signaling pathways, under both normal cultural condition and starvation (Figure 1(d)). The gene discussed is AKT1; the disease is neoplasm.