After the emergence of SARS-COV2 in Wuhan, a strain was evolved with more infective power (8). Genomic analysis shows that this strain bears a nonsynonymous mutation (D614G) at the S1/S2 boundary that can generate extra TMPRSS2 serine protease cleavage site (9). However, it is predicted that people with an SNP (Del C) at the intergenic region between TMPRSS2 and MX1 gene apparently are infected more as this deletion is prevalent in Europe and United states and also in Indian subcontinent than other parts of the world (MAF, Minor Allele Frequency of Caucasian (CEU) 0.49; Indian 0.35; African, 0.005 and Chinese, 0.006; www.ensembl.org). This SNP is in cis- eQTL for both TMPRSS2 and MX1 gene and increase their expression in human lungs and other tissues [Fig.2 ]. Further analysis suggests that this SNP region is H3K27AC layered (ucsc.genome.edu) with regulatory region. Hi-C interactions confirms this region contains a TAD (Topologically Associated Domain) and promote interaction of this SNP region with MX1 and TMPRSS2 promoter [Suppl. materials 3A ]. The flanking region of this SNP contain two regulatory motifs – a CTCF binding region and promoter flanking region. Immediate flanking nucleotides consist of a protein binding motif (GWAAATGA) [Fig.3B, Suppl. Materials 3B ]. Most conspicuous feature is that 300bp flanking sequences of this SNP are identified at several genomic locations implying that these sequences may act as a global regulatory element [Fig.3A, Suppl. Materials 2 ]. It appears that Del C SNP is a strong regulatory element and modulate the expression of TMPRSS2 and MX1 gene and these proteins may have a major role in controlling the infectivity of SARS-COV2 in Caucasians and Indians. With extensive experiments, recently Zhang et al (2020) showed that 614G mutated protein increase the number of binding sites by shedding the S1 protein and increase infectivity(10).