Beyond nuclear hormone receptor-based synergy, the PI3K pathway has been shown to positively regulate FOXP1 expression and its downstream transcriptional effects33; FOXP1 deletion in the context of PTEN loss therefore allows tumors to circumvent the induction of tumor suppressive FOXP1-mediated transcriptional activity, which would otherwise result from PTEN loss-mediated PI3K activation. Here, NR0B1 is linked to neoplasm.