The observed RNA-mediated competition with membrane clustering suggests a dynamic regulation of 2C functions during viral infection. Initially, 2C facilitates membrane clustering to create a conducive environment for viral replication. However, as RNA, particularly double-stranded RNA, accumulates during replication, it competes with membrane clustering, potentially signaling a shift in 2C's role. This competition may serve as a temporal regulatory mechanism, allowing 2C to transition from membrane clustering to assisting RNA replication and particle assembly. The ability of RNA to outcompete membrane clustering highlights the intricate interplay between different stages of the viral replication cycle and the adaptability of 2C in response to changing intracellular conditions.