In our current model, KCa3.1 blockade using senicapoc, a drug very well tolerated in a phase 3 clinical trial of human sickle cell disease, was highly effective at inhibiting the pro-fibrotic effects of TGFβ1 both in terms of gene transcription, and tissue protein markers of fibrosis. This evidence concerns the gene TGFB1 and sickle cell disease.