The purpose of our study was to determine if direct administration of CXCL1/KC to cardiomyocytes causes negative changes to cell density or proliferation. This molecule has been shown to reduce inflammation in certain instances. Homocysteine models the direct effect of an inflammatory agent on cardiomyocytes. Our question was whether these molecules directly impact cell density through an interaction with the cell proliferation process. We hypothesized that cells treated with CXCL1/KC would maintain the same cell density as untreated cells. In contrast, cells treated with Homocysteine or both Homocysteine and CXCL1/KC, were expected to have a higher cell density that than that of untreated cells. To test these hypotheses, HL-1 cardiomyocytes were cultured and treated in chambers on a glass slide. DAPI staining, which allows individual nuclei to be counted, was viewed under fluorescence and pictures were analyzed using Image J. Our hypotheses were rejected because there was a significant difference between the Homocysteine group and both the Homocysteine+CXCL1/KC and CXCL1/KC groups. This was extended to signify that the cell density of the CXCL1/KC and Homocysteine+CXCL1/KC groups was decreased cell proliferation had been reduced. The difference between the CXCL1/KC and Homocysteine groups likely indicates effects possessed by each treatment. Comparing results from the Homocysteine+CXCL1/KC treatment to the Homocysteine treatment, Homocysteine treatment increased cell density enough so that the decreased proliferation which may have been caused by the CXCL1/KC was significant compared to the Homocysteine sample. Future studies could examine additional applicable models such as mouse heart tissue or a living mouse.