Notably, low-risk types such as HPV6 obviously prefer the mode of gene suppression instead of post-translational labilization of the IL-1β precursor protein to escape immune surveillance (see Fig. S4B), since five out of five genital warts showed a complete shut-off in IL-1β transcription when compared to primary keratinocytes which were used as a positive control (Fig. S4C). The gene discussed is IL1B; the disease is anogenital human papillomavirus infection.