Further, by over-expressing PC2N and PC2C in human melanoma A7 cells we found by co-IP that both PC2N and PC2C interact with endogenous FLNA and that the PC2N-FLNA interaction is stronger than the PC2C-FLNA interaction (Fig. 3C), in agreement with our results obtained from in vitro binding data (Fig. 1 and 2). The gene discussed is FLNA; the disease is melanoma.