At subtoxic concentrations, H2S has been shown to stimulate ATP production at the level of oxidative phosphorylation, both as a source of electron equivalents for the mETC (via SQR-mediated quinone reduction, Table 1), and through per-sulphidation of ATPase, which maintains the enzyme in its activated state.146 Szabo et al.52 reported that increased oxygen consumption by mitochondria isolated from colorectal cancer HCT116 cells treated with cysteine was suppressed upon CBS inhibition. This evidence concerns the gene CBS and colorectal cancer.