Importantly, immunoprecipitation of the mutant GFP-liprin-α1-AA reduced the binding of endogenous B56γ as well as of PP2A-A and PP2A-C (Fig. 1k), suggesting that B56γ is the main regulatory subunit mediating the interaction of liprin-α1 with the PP2A holoenzyme in MDA-MB-231 tumor cells. The gene discussed is PPP2R5C; the disease is neoplasm.