Accordingly, the MCU-upregulated PGC-1α promoter activity was augmented by the overexpression of MKK6-CA (a constitutively active mutant of MKK6) and suppressed by the overexpression of p38α-DN; and (5) in THP-1 cells (human monocytic leukemia cell line), MCU-mediated ROS production in the macrophage mitochondria was abolished by the silencing of Rieske, the iron–sulfur protein in complex III, which showed good parallelism with a marked inhibition of the p38/ATF-2-signaling axis and PGC-1α expression [105]. This evidence concerns the gene PPARGC1A and monocytic leukemia.