Most of the human genome—close to 99%—is composed of noncoding DNA that does not code for proteins. Despite this sequence majority, relatively little is known about noncoding DNA relative to protein coding DNA. Historically, there has been little agreement as to what even constitutes functional cis-regulatory elements (CREs, such as promoters and enhancers). This is in part due to the fact that though features such as histone mark and transcription binding are correlative, they are not necessarily causative. In addition, some CREs act redundantly and in combination, and many methods to study them do not consider the element in its native context (e.g. massively parallel reporter assays [MPRAs]). Regardless, these CREs act to finely tune the expression of their target genes, and a disease context, learning how to curb the action of CREs can have big therapeutic implications. In this work, I use CRISPR screens to study the noncoding regulation of an oncogene across multiple cancer types.