Based on these observations, it was proposed that for enteroviruses either another viral protein(s) is required to co-operate with 3A to increase PI4KB activity during infection [107] or, alternatively, that ACBD3 could provide a scaffold function for the correct positioning (and function) of 3A in the RC/RO, rather than serving to recruit active PI4KB [307]. The gene discussed is PI4KB; the disease is infection.