In addition, MCT1 knockdown via lentivirus infection of specific shRNAs remarkably abrogated the effects of reconstituting wild-type KAT2A in RCC cells (Caki-2 and A498) in which KAT2A had been knocked out, indicating that KAT2A depended on MCT1 to promote RCC proliferation (Figure 5D). Here, SLC16A1 is linked to infection.