In this respect, immunoprecipitation-based studies suggested a BRM-ADNP interaction coupled to ADNP-polypyrimidine tract-binding protein (PTB)-associated splicing factor (PSF) binding, with PSF being a direct regulator of Tau transcript splicing [76] and with Tau deposition (tauopathy) being noted in both Adnp+/− [77] and Tyr mice [22], as well as in ADNP syndrome post-mortem tissue [9]. The gene discussed is SMARCA2; the disease is ADNP-related multiple congenital anomalies - intellectual disability - autism spectrum disorder.