We previously identified two linked SNPs in the MAVS gene that render the MAVS protein insensitive to the PLK1-dependent HIV-1 evasion mechanism and it was shown that untreated HIV-1-infected individuals homozygous for the minor alleles (MAVS minor genotype) contained a decreased viral load at set point and prolonged control of viral replication during the course of HIV-1 infection [15]. The gene discussed is PLK1; the disease is HIV-1 infection.