Figure EV4. MCL1 inhibitors.

1. Correlation of all MCL1 inhibitor IC₅₀ values against MCL1 and MARCH5 gene fitness profiles. Effect sizes (b) and FDR (P) of the association are reported on the bottom.
2. Stratification of the MCL1 inhibitors drug response measurements according to the cell line dependency on MARCH5 and/or MCL1. Gene vulnerabilities are independent from each other, meaning knockouts were introduced independently and not at the same time. Responses are then split according to the cancer type of the cell lines. Number of measurements per boxplot are: acute myeloid leukaemia (MCL1 = 3, MCL1 + MARCH5 = 2, None = 1), breast carcinoma (MARCH5 = 2, MCL1 = 9, MCL1 + MARCH5 = 4, None = 14) and Other (MARCH5 = 9, MCL1 = 52, MCL1 + MARCH5 = 21, None = 236). Vulnerable cell lines to MARCH5 and MCL1 knockout were defined as those with a depletion of at least 50% of that visible for essential genes on the particular cell line (scaled log₂ fold change < −0.5). Grey dashed line represents the maximum concentration used in the dosage response curve of the respective drug. Box‐and‐whisker plots show 1.5× interquartile ranges and 5–95^th percentiles, centres indicate medians.
3. Representative example of a MCL1 inhibitor and their relation with MCL1 gene fitness, with cell lines containing copy number amplification of MCL1 highlighted in orange. Copy number amplified cells were defined taking into consideration their ploidy status, cells with (ploidy ≤ 2.7 and copy number ≥ 5) or (ploidy > 2.7 and copy number ≥ 9) were considered as having MCL1 amplified. Box‐and‐whisker plots show 1.5× interquartile ranges and 5–95^th percentiles, centres indicate medians.