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The study was retrospective including all requests for PNH clone research received at the flow cytometry laboratory of the CRTS of Sfax over a period spanning from 2004 to 2017. For each patient and/or witness of the day, a sample of peripheral venous blood was taken on tubes containing EDTA and was sent directly to the laboratory. The search for the PNH clone by CMF consisted of analyzing the expression of GPI-anchored molecules: CD16 and CD66b on granules and CD14 on monocytes. The presence of a HPN clone was retained when at least two cell populations (monocytes and PNNs) presented a deficiency in the expression of GPI-anchored molecules. The deficit threshold for GPI-anchored molecules was set at 5%.In our series, 12 cases of PNH clone were diagnosed and the CD14 expression deficiency was 25% (5.1-91%). That of CD66b and CD16 were 44% (5.2-100%) and 36% (0-94%) respectively.