This discrepancy in thedecrease in VACV replication upon inhibition of the ACAT and DGAT in differentcell lines further highlights our assumption that modulation of the lipiddroplet synthesis during VACV infection could be cell-type dependent and thatdifferent cell types could react differently to the virus infection.Nevertheless, these findings highlight the importance of the synthesis ofneutral lipid droplets in VACV replication in primary HFFs. The gene discussed is SOAT1; the disease is viral infectious disease.