Moreover, this study documented that the absence of Rictor led to the overexpression of chemotaxis-related proteins, such as CCR2, CCR4, and C-X-C chemokine receptor (CXCR) 4, which most likely contributed to increased migration and the homing of Rictor-deficient T-ALL cells to the spleen, whereas migration to bone marrow was negatively affected. Here, RICTOR is linked to acute lymphoblastic leukemia.