Inositol 4-phosphatase which mainly acts on phosphatidylinositol 4-phosphate. May be functionally linked to OCRL, which converts phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol, for a sequential dephosphorylation of phosphatidylinositol 4,5-bisphosphate at the 5 and 4 position of inositol, thus playing an important role in the endocytic recycling (PubMed:25869668, PubMed:25869669). Regulator of TF:TFRC and integrins recycling pathway, is also involved in cell migration mechanisms (By similarity). Modulates AKT/GSK3B pathway by decreasing AKT and GSK3B phosphorylation (PubMed:17322895). Negatively regulates STAT3 signaling pathway through inhibition of STAT3 phosphorylation and translocation to the nucleus (By similarity). Functionally important modulator of cardiac myocyte size and of the cardiac response to stress (PubMed:19875726). May play a role as negative regulator of axon regeneration after central nervous system injuries (PubMed:26203138). a myo-inositol phosphate + H2O = myo-inositol + phosphate Homodimer (By similarity). Interacts with OCRL and RAB5. Interacts with INPP5B and INPP4A (PubMed:25869668). Interacts with STAT3; the interaction is independent of STAT3 'TYR-705' phosphorylation status (By similarity). Also found on macropinosomes. Highly expressed in brain and hypothalamus, expressed in lung and pancreas, and detected at low levels in liver and heart (at protein level). Up-regulated in the absence of histone deacetylase 2/HDAC2 in the heart from HDAC2-null mice. Animals develop normal corticospinal tract and raphespinal tract. Mutants show greater axonal growth and functional recovery after central nervous system trauma (PubMed:26203138). Knockout mice have normal cardiac form and function but show augmented hypertrophy and reactivation of the fetal gene program in response to stress compared to wild-type littermates (PubMed:19875726). INPP5F has been initially described as an inositol polyphosphate 5-phosphatase.