HCV-related LPD pathogenesis is a multifactorial and multistep process. Current data suggest that the starting points of this process are represented by the cooperation between a sustained and persistent stimulation—by direct or indirect action of viral particles or proteins—and antiapoptotic mechanisms acting on B-cell compartment. A predisposing genetic background would be responsible for the final evolution to a particular LPD (namely, MC). The progressive addition of genetic aberrations would lead to a frank neoplastic transformation, gradually making the process less dependent on the etiologic agent.
