The emergence of artemisinin resistance in SEA has resulted in focused attention to this region to avert possible spread to SSA. The K13 mutations are mostly localized in small geographical area in SEA where they originate independently and have particular genetic background. Some of these mutations have also been identified in SSA parasites, but without the delayed clearance phenotype. NS K13 mutations are undergoing strong evolutionary selection in SEA but not in SSA. We evaluated the status of artemisinin resistance in SSA by analyzing the K13 mutations. Data reported here is from 10 countries representing east, west and central African nations with different transmission intensities and are geographically dispersed. ~1300 Pf samples were whole genome sequenced on Illumina. Additional 315 samples from ACT efficacy studies in Kenya were sequenced on Sanger. Despite the presence of sustained high infection complexity, low linkage disequilibrium and high recombination, NS K13 mutations were present in low frequencies and none of the WHO validated K13 resistance mutations were present. Population structure analysis revealed presence of distinct east African, Ethiopian and west African parasite populations. Ethiopian isolates were significantly divergent from all other populations. Analysis of the drug resistance SNPs resulted in loss of the east-west geographical sub-division of the parasite population structure. There was no evidence of drug resistant gene flow from east to west Africa which is against the popular dogma of east to west gene flow, where resistant parasites migrate from SEA to SSA. K13 mutations in SSA are private, emerge locally, are not under positive pressure, and do not confer artemisinin resistance. The K13 mutations and frequency differ even inside each country, and K13 mutations were present in pre-ACTs parasites. There is no evidence that artemisinin resistant parasites from SEA are likely to flow to SSA, using the east to west route.