Previously reported Akt-independent mechanisms of PTEN tumor suppression include the regulation of a PTEN dependent cell size checkpoint [33], activation of JNK signaling pathways [35], activation of SRC signaling via PTEN protein phosphatase activity [36], phosphatase independent PTEN protein-protein interactions regulating the PKR-eIF2α phosphorylation pathway [37] and the oncogenic transformation of cells by MSP58 [38]. Here, SRC is linked to neoplasm.