It activates JAK/STAT signalling, inducing transcription of inflammatory and pro‐fibrotic genes such as APOL1, which is strongly associated with increase the risk of kidney damage, including fibrosis, leading to chronic kidney disease (CKD) and potentially kidney failure in individuals of West African descent carrying the G1 or G2 risk variants [9–11]. This evidence concerns the gene APOL1 and Nephropathy.