BACH1 depletion activates the expression of several cytoprotective genes which explains why BACH1 appears as an attractive therapeutic target against a variety of inflammatory and oxidative stress-related conditions including Huntington's6 and Parkinson's disease [7], sickle cell disease [8], ischemia/reperfusion injury [9,10], non-alcoholic steatohepatitis [11], insulin resistance [12], coronary artery disease [5,13] and tuberculosis infections [14]. This evidence concerns the gene BACH1 and sickle cell disease.