Following infection, let-7c, miR-34a, or miR-124 was upregulated, and they targeted and downregulated p21 and TASK1, which eventually led to increased virion release and higher copy number of viral genome transcripts in infected cells, suggesting that HIV-1 could utilize the host miRNA cellular systems to produce a more efficient infection process via blocking the mechanism of innate inhibition (54). Here, KCNK3 is linked to infection.